Sunday, October 18, 2015

No KCAL9, that's not what the results mean. Part 4

Okay Bowman, you are confusing me.  How can 101 mg/kg of lead in the soil possibly make it a hazardous waste, but 400 mg/kg in the soil make it acceptable for children to live at?

That don't make no sense!

What makes a physical solid material a hazardous waste for lead is based on the idea that if the lead leaches out at or above 5 mg/L it could get into the groundwater and be consumed above the maximum contaminate level (MCL).
The STLCs and TTLCs, originally proposed in 1978, were intended to identify those wastes that “pose a substantial threat to human health and the environment if not disposed in a controlled and systematic manner.  ...the STLC for lead focused on ingestion of drinking water as the route of exposure, considering the exposure pathway of drinking water derived from groundwater or surface water. The STLC was developed by applying a 100-fold attenuation factor to the maximum contaminant level (MCL) for lead, which was 50 µg of lead/L of drinking water at the time the threshold was developed. (Page 4-4)
What makes soil containing less than 400 mg/kg of lead "not hazardous" is based on a risk assessment related to children and the concentration of lead in the blood.

The idea that 5 mg/L of lead leaching from soil is hazardous is archaic. But it is how the regulations require a determination of "hazardous waste" be met.  Would soil that leaches out 5 mg/L of lead create a hazard for the public - children in particular - ??  I don't know.  My guess is that based on what we know now, probably not.

But you are more interested in why up to 400 mg/kg of lead in the soil is okay for a backyard where children play.

That value of 400 mg/kg is based on a complex risk assessment, which is based on how much lead would increase the blood-lead level in a child:
Briefly, within the context of the §403 risk analysis, individual risks refer to the risks associated with a young child’s exposure to specified levels of environmental-lead. Once environmental-lead levels were specified for each medium, the model-predicted blood-lead concentration at these levels, along with the assumption that blood-lead concentrations have a lognormal distribution with a specified variability, were used to estimate the percentage of children exposed to the specified set of environmental-lead levels that would have elevated blood-lead concentrations (i.e., at or above 10 µg/dL). 
Then, those sets of environmental-lead levels associated with estimated elevated blood-lead percentages of 1%, 5%, and 10%... The IEUBK model was used to identify soil-lead concentrations associated with these elevated blood-lead percentages (at specified dust-lead loadings), while the Rochester multimedia model was used to identify (wipe) dust-lead loadings associated with these elevated blood-lead percentages (at specified soil-lead concentrations).  (source)
Told you it was complex!

California looks at lead a bit differently than the EPA, which offers even more confusion when trying to understand why.
One of California’s hazardous waste standards is the total threshold limit concentration (TTLC). The TTLC for lead is intended to protect receptors from direct exposure, primarily through ingestion, which is the type of exposure of greatest concern with lead and certain sensitive receptors. The TTLC in use today assumes that 1,000 mg/kg is protective of children likely to ingest soil containing lead. However, as shown by the recently developed health-based screening values for soils at school sites and near residential lead-paint sites, soil-lead concentrations that protect children who are exposed to lead in soil range from 255 mg/kg to 400 ppm, depending upon the model and assumptions used. The models and assumptions used to develop these values consider the most recent information regarding the health effects of lead and the exposure likely to occur.
California lowers that threshold to 80 mg/kg for children:
The Department of Toxic Substances Control’s Leadspread model (DTSC, 2007) was used to estimate blood lead concentrations in children. The Leadspread model considers exposure to lead in soil by three pathways: ingestion, re-suspension and inhalation, and dermal contact. The Leadspread model was queried for the soil lead concentrations that would give rise to a 90th percentile estimate of increase in blood lead of 1 µg/dL using the “goal seek” function in Excel
The point of all this is this.  The lead concentrations Randy Paige found using the XL2 XRF are above 400 ppm.  This is concerning, especially if the California model is correct.

What needs to happen now is to look at the blood-lead levels in these children.  That would indicate the potential for health concerns.

No need to scare people with "hazardous waste."  That's a whole different wacky world that does not apply to these folks living in Vernon near the Exide facility.

tl;dr: Stop saying "hazardous waste"!!


Thanks for reading.

Jeff


No KCAL9, that's not what the results mean. Part 3

Is soil that contains 1000 ppm of lead - as detected by a Niton XL2 XRF - a hazardous waste?

Probably not.  But I cannot say for sure without running a TCLP on the soil.

But it contains 100 ppm of lead!  The regulatory limit for lead as a hazardous waste is 5 ppm!  That's 200 times more lead in that soil than a hazardous waste!

Whales are aquatic.  Fish are aquatic.  Whales are not fish.

XL2 XRF reports a ppm for lead.  TCLP reports a ppm for lead.  These ppm results mean two different things.  You cannot use the XL2's ppm to state "hazardous waste."

And here is where it gets really wacky!

The XL2 is telling us a ppm based on surface area and depth.  I do not know how this correlates to a ppm we use in environmental determination of regulatory compliance or cleanup levels.  I am going to assume that the ppm reported aligns with mg/kg - the standard way we discuss ppm when looking at lead in soil.

So let's just accept that a reading of 1000 ppm determined by Randy Paige when using the XL2 in the yard near the bike detected 1000 mg of lead per kg of soil.

1000 mg is 200 times more than 5 mg (the hazardous waste threshold).

Yeah...but..1000 mg per kilogram of soil versus 5 mg per liter of liquid (the leachate).

They do not correlate.  With one exception...

If we were to run a totals constituent analysis on that soil, and we obtained 1000 mg/kg of lead, this would cause us to consider the soil as possibly being a hazardous waste.  This is due to a concept we call "the rule of 20."
If a waste is 100% solid, as defined by the TCLP method, then the results of the total constituent analysis may be divided by twenty to convert the total results into the maximum leachable concentration. This factor is derived from the 20:1 liquid-to-solid ratio employed in the TCLP.
So now we have ourselves a dilemma.

If the ppm reported by the XL2 correlates to a totals analysis result in mg/kg.  1000 ppm detected by the XL2 is way above "the maximum theoretical concentration in the leachate could have" which is 20 times the TC regulatory value of 5 mg/L - or 100 ppm.

If the soil contains less than 100 ppm of lead from a totals analysis, then theoretically, because of the 20 to 1 dilution - it could not leach more than 5 mg of lead per liter of leachate.

Too many numbers Bowman!  Boring!

Okay...so work with me here.  We are told 1000 ppm in the backyard by the bike. Let's assume that 1000 ppm reported by the XL2 meter is the same result we would get if we took a soil sample to a laboratory.  1000 ppm is greater than 100 so we cannot rule out this soil - in this backyard - by this bike - does not meet the definition of a hazardous waste.

Here we get wacky!

The EPA threshold for lead in the soil of residential property is 400 ppm.

But...400 is four times higher than 100 - the theoretical value!  How can the EPA say that up to 400 ppm is a safe level for children?

Because what makes something a hazardous waste relates to risk of a particular health impact and not the health impact that is present.

Confused?


No KCAL9, that's not what the results mean.  Part 4

No KCAL9, that's not what the results mean. Part 2

Using the term "hazardous waste" in this report was done - and I am being qualitative here - to illicit a much more visceral response from readers and that community.

Or, Randy Paige - the reporter - was misinformed about what makes lead in soil a hazardous waste

Or, Randy Paige just completely does not understand what a hazardous waste is and uses the term because he thinks it is appropriate.

The reason I started this blog - and the reason it is called the Wacky World of Waste - is because hazardous waste is, well, wacky.

If you think that calling something a "hazardous waste" somehow elevates it to a new level of concern you would be wrong.

Here are a four examples of hazardous waste:

D001 Ignitable Hazardous Waste -  fire through friction 40 CFR 261.21(a)(2)

and this...

U129 Toxic Waste  - 40 CFR 261.33(f)

and this one...
D001 Ignitable Hazardous Waste - 40 CFR 261.21(a)(3)

and this too...

D003 - Reactive (Flame-less Ration Heater [FRH]) - 40 CFR 261.23(a)(3)

 My mom takes Coumadin as a blood thinner.  Coumadin contains warfarin which is an acutely hazardous waste - P001.

So calling something a hazardous waste means what?

Wacky right?

But let's get back to the soil with lead as a hazardous waste, shall we.


Next post: No KCAL9, that's not what the results mean.  Part 3

No KCAL9, that's not what the results mean. Part 1

Argggggg.

CBS2/KCAL9 rented a device certified by the EPA to provide instant readings of the amount of lead in soil or dust.
If you read any of my posts, you know I get all long-winded about methodology and technique.  I don't want to go that route with this post.  So I will ignore this screenshot from the video:


Now I don't know much about XRF analyzers, but I stayed at a Holiday Inn Express once, so that taught me how to Google.

Google brought me to the Thermo Fisher Scientific Niton Analyzer website - the guys who make the instrument shown in the screenshot.

That looks to be a Niton™ XL2 XRF Analyzer, which, when I click on the link "Which XRF analyzer is right from me?" I am shown this:

Source

The reason I need to ignore that table that shows which instrument is used for what matrix, is because of this statement:
We found levels more than 10 times that amount with so much lead in the soil, it was defined as hazardous waste.
I don't want to split hairs on if the XL2's results are accurate and they should have used an XL2 GOLD for sampling soil.  I don't want to discuss if this reporter - the guy shown using the instrument - was trained to use it.  I will ignore the requirement from Thermo - as detailed by USA Today in a report they did on lead in the soil near smelters - that "to be considered a valid test result...a full 80-second scan had to be completed" because the results shown were under 80 seconds.

I am going to ignore all of that and accept the values the reporter tells us the instrument determined are accurate.

Instead I want to focus on these statements:
...it was defined as hazardous waste.
and this statement:
... contained hazardous-waste levels of lead...
and this:
...we found levels of hazardous waste...
and this:
...was exposed to this hazardous waste.
and this:
...it, too, is defined as hazardous waste.
and this too:
...such high levels of hazardous waste...
What makes soil containing lead a hazardous waste is dependent on the amount of lead that leaches from the soil.  The reporter is using the XL2 for an in situ soil sample that is qualitative, not quantitative.

The instrument reports ppm that is based on this:
The FPXRF instrument measures the metal content of the sample over a surface area of approximately one square centimeter (1 cm2) to a depth of approximately 2 millimeters (2 mm), displaying lead concentration in parts per million (ppm). (US EPA)
To be defined as a hazardous waste, soil containing lead must be tested using a procedure called the "Toxicity Concentration Leaching Procedure (TCLP) which reports the concentration of lead as mg/L.

The reading you get from the XL2 - reported in ppm - does not equate to the concentration you would get running a TCLP on that same soil sample.

You can state we found levels of lead in the soil measured at 1,000 ppm but you cannot state "we found levels of hazardous waste measured at 1,000 ppm."

A determination of hazardous waste is a different animal than reporting a screening level.

And here is where it gets wacky...

Next post: No KCAL9, that's not what the results mean.  Part 2

Sunday, September 13, 2015

Breast Milk and PFASs - Part 10

Back to the real focus.

Remember why the Breastfeeding Paper authors focused on PFASs as a health concern.
...a major concern is that PFAS exposure may undermine childhood immunization programs.
Remember the paper they cited to substantiate that concern; the Antibody Paper.

Now remember what the Antibody Paper authors said about the maternal serum concentration at week 32 of pregnancy.
The prenatal exposure level, as indicated by the mother’s serum concentration during pregnancy, was less clearly associated with the antibody outcomes.
The Antibody Paper tells us this:
In a structural equation model, a 2-fold greater concentration of major PFCs in child serum was associated with a difference of −49% (95% CI, −67% to −23%) in the overall antibody concentration.
This is based on looking at the PFASs at age 5 and 7 years and comparing them to the antibody concentrations found.  Doubling the amount of PFASs was shown by their model to decrease the overall antibody concentration by about 50%.

Let's look at the reality of that population of 656 in the study.  After 5 years, 532 children showed this level of antibody concentrations prebooster:

Source: Antibody Paper - Table 1 excerpt

For tetanus, 75% of the values for the 532 children were above 0.1 IU/mL which we are told:
...is considered an important indicator of protection in accordance with the public health rationale for routine vaccinations.
75% of all these children had antibody concentrations above the protective level for tetanus and almost 75% of these children had antibody concentrations above the protective level for diphtheria.

That is 75% for of the 532 children from the Faroe Islands who were specifically chosen for this study because:
frequent intake of marine food is associated with increased exposures to PFCs
If 75% of these kids with a suspected increased exposure to PFASs for both them and the mother are protected (above 0.1 IU/mL), then what would we expect the antibody concentrations to be in a child born to a mother in San Antonio, Texas?

Even if the Antibody Paper's model is true, and we see a 50% reduction in antibodies with a 2-fold increase in exposure to PFASs, Does breastfeeding there in the Faroe Islands or in San Antonio, Texas produce a 2-fold increase in PFASs for the child?

Does 6 months worth of breastfeeding produce a noticeable increase in PFASs whereby the antibodies would decrease below the 0.1 IU/mL protection level?  Is there a statistical difference between children who are breastfed falling below the 0.1 IU/mL protection level compared to children who were not breastfed.

That's the question they should have asked and that's the statistics they should have reported.

Armed with that, one could then decide to forgo breastfeeding benefits in order to reduce the chance of their child falling below the antibody protective level of 0.1 IU/mL.

Every time I read the Breastfeeding Paper I came up with more" huh?"  Things I needed to know were left out.  When I realized just how how off the mother's serum concentrations were from the population of mothers they were pulled from, the paper's findings became less and less credible.

Here is what I know from the Breastfeeding Paper:

They have 81 mothers and those 81 mothers have 81 children.  From this 81 they were able to get data.

Ignoring the mother's serum levels reported for PFOS, we see that 68 children from these 81 mothers had their blood tested at age 11 months.  We are shown data that tells us how much PFOS were in the kids at 11 months.

We also have data for PFOS in these kids at 18 months.  We are not told if these are the same kids from testing at 11 months, or a new set of the kids from the 81 tested at 18 months.

We are told this:
Figure 1 shows the trajectories of the five major PFAS for the 12 children with complete observations from all examinations.
What I understand this to mean is that only 12 children of the 80 mothers had blood sampled for PFOS at 11 months and 18 months.

We are told that the amount of time some of these 81 children were exclusively breastfed was 4.5 months.  We are told that some of these 81 children were partially breastfed for 4 months, and that some of these 81 children were only breastfed for one month or less.

What we are not told is how many of the 73 women of the 81 who replied to the question on breastfeeding fall into each of those three groups.

What were are not told is' of the 73 women of the 81 who replied to the question on breastfeeding, what the concentration of PFOS for each of these three groups.

What we are instead given is a graph:

Source: Breastfeeding Paper - Figure 1

We are told by the authors of the Breastfeeding Paper this:
The child with the lowest concentrations (blue dotted line) was not breastfed at all, whereas the child with the highest PFOS concentration (black solid line) was breastfed exclusively in 6 months and was partially breastfed during the following 5 months.
What we are not told - and I have looked and looked to make sure I did not overlook it - is what the other lines and colors represent.  That bit of information was left out.  Oops!

Okay, you got 12 kids with complete data.  One of them was breastfed exclusively and the other was not.  Does the blue dotted line represent the population of those who do not breastfeed?  Does the black solid line represent the population that exclusively breastfeeds?

What do the other lines show?

Here is what I want to know:

  1. What was the concentration of PFOS at 11 months for the kids who were exclusively breastfed?
  2. What was the concentration of PFOS at 11 months for the kids who were not breastfed?
  3. What was the concentration of PFOS at 18 months for the kids who were exclusively breastfed?
  4. What was the concentration of PFOS at 18 months for the kids who were not breastfed?

With that data, one could see if there is a statistical difference between the two groups.  Why was that not done?  Why focus on showing us a graph of 12 of them and leave out the explanation of the data for 10 of those 12?

I am unwilling to look at two children and say that their PFOS values represent the two groups.  In particular, the PFOS values for the not breastfed kid - the blue dotted line - is way below the lowest IQR reported for 68 of the kids tested at 11 months.

So there you have it.  I have beat this dead horse as much as I can.

If you are going to forgo the benefits of breastfeeding because you are concerned about passing on PFASs to your baby, then you would be making a big mistake if the reason for doing so is based on this paper's findings.

Thanks for reading.

Breast Milk and PFASs - Part 9

Continuing on from my last post...

In order for me to be correct in what I am about to show, my observation of the Breastfeeding Paper data must show that a geometric mean and IQR they used in their model is what I am seeing and was used to produce this statement:
The duration of exclusive breastfeeding was associated with increases of most PFAS concentrations by up to 30% per month, with lower increases during partial breast-feeding.
According to the Breastfeeding Paper's authors, the serum concentration for PFOS for the 80 mothers had a geometric mean of 6.0 ng/mL and an IQR of 5.2, 7.2.  This, if my understanding of an IQR is correct, means that 75% of the PFOS found in these 80 mothers was below 7.2 ng/mL.

Source: Breastfeeding Paper - Table 1 excerpt

Those 80 mothers were pulled from the 656 mothers with serum concentrations of PFOS collected at week 32 of pregnancy.

Here is where my angst is coming from.  Let's look at the data presented in the Antibody Paper for the 656 mothers from which those 80 mothers were pulled from:

Source: Antibody Paper
In particular, lets just look at the serum concentration for PFASs found in the 656 mothers at week 32 of pregnancy.


Source: Antibody Paper - Table 2 excerpt

Notice something?  The Antibody Paper from which the data came from tells us that the PFOS in the 656 mothers tested have a geometric mean of 27.3 ng/ml.

Something ain't right here.  How can these 80 mothers - pulled from the 656 mothers - have a PFOS serum concentration that far below the lower IQR of 23.2 ng/mL?

75% of the 80 mothers have a PFOS concentration in the lowest 25% of the 656 mothers?

That's...that's...highly unlikely!

In fact, looking at their data in Table 1, almost all of the four PFASs upper IQR value for the 80 women are below the lowest IQR value reported for the 656 women they came from.

That cannot be correct.  The odds of 80 mothers being so drastically different from the population they came from would, without benefit of a calculation, be exceptionally low, I contend that this serum data from the mothers is in error.

In contrast, the PFASs reported for the children at 11 months and 18 months fall very close to the IQR range reported for the mother's 32 week pregnancy concentration in the Antibody Paper.

Source: Breastfeeding Paper - Table 1 excerpt

At 5 years (60 months) the PFASs of these 80 kids align very close to the results report for the 656 in the Antibody Paper.

Source: Breastfeeding Paper - Table 1 excerpt

Source: Antibody Paper - Table 2 excerpt

I contend - and I could be wrong here - that the values they used in their prediction model for 0 month - the serum concentration of PFASs at 32 weeks of pregnancy - for these 80 mothers is incorrect.  I cannot accept the ng/mL values for 0 month that they report in Table 1.  I cannot accept it based on what is reported for the overall population for the mothers in Table 2 of the Antibody Paper which is where these 80 mothers came from.

If the glove don't fit....

So...the Breastfeeding Papers claims to show that:
The duration of exclusive breastfeeding was associated with increases of most PFAS concentrations by up to 30% per month, with lower increases during partial breast-feeding.
But for that to be true, the actual serum level of the child would need to be known at 0 month.  If you are going to assume that the serum level of the mother at 32 weeks is that value, then that value must be correct for your model to be sound.

Here is what I see - and why it has taken me a while to write these last posts.

I see that 328 women from the Antibody Paper had blood serum concentrations of PFOS between 23.2 and 33.1.  That's a range of 9.9 between 328 women.

According to the Breastfeeding Paper, 60 of the women - pulled from the Antibody Paper's 656 women - had PFOS concentrations 20.1 less than the lowest value seen in 492 (75%) of the women tested.

That cannot be correct.

Next post: Part 10

Breast Milk and PFASs - Part 8

The posting for a conclusion to all of this is taking me longer than I anticipated.  I'll explain why in a bit if you keep reading.

Focus: Should a new mother forgo the benefits of breastfeeding based on the findings based on the findings present in this paper:
Breastfeeding as an Exposure Pathway for Perfluorinated Alkylates
This paper made my Google Newsfeed show me news articles with titles such as this:
Breast milk may be tainted with toxic chemicals – says new research
The authors of this paper, which from here on I will call the "Breastfeeding Paper," tell us in the abstract that:
The duration of exclusive breastfeeding was associated with increases of most PFAS concentrations by up to 30% per month, with lower increases during partial breast-feeding.
That "30% per month" statement is the result of their modeling:
We first included only the three concentrations obtained at birth and at age 11 and 18 months. The model was estimated using a linear mixed model with breastfeeding variables included as covariates.
What is important to understand at this point, is that the amount of PFASs in the breast milk was never measured:
However, neither the newborn baby’s PFAS concentrations nor the concentrations in milk were measured in this study, which instead relied on the maternal serum concentrations measured at a specified point during pregnancy/
The concentration used in their model for month 0 is this:
Serum-PFAS concentrations at birth were calculated from maternal concentrations.
Month 0 is critical for their model, which uses three points for their prediction, 0 month, 11 months, and 18 months.  This is where the statement "increases of most PFAS concentrations by up to 30% per month" comes from and is shown in their prediction graphs.

Source: Breastfeeding Paper

Here is where I started to have troubles and why it is taking me a while to get these posts out.

I need to make sure that what I see is correct before I put it out for the whole world to see.  I understand I could be wrong in anything I post.  I admit that, and I will correct my mistakes if they are pointed out.  I want to be objective and fair.

I am trying to have my facts straight and my understanding of what I see as sound as I can get it before I post it for all the world to see.  So here goes.  If I am mistaken from what I post, I will apologize and I will correct it.

Let's get back to month 0 in their model.
Serum-PFAS concentrations at birth were calculated from maternal concentrations.
Where did this data come from?
A birth cohort of 656 children born in the Faroe Islands was formed during 1997−2000 and followed prospectively. A serum sample and informed consent were obtained at week 32 of pregnancy.
Hmmmm.  That's the same cohort used in the paper they cite for "vulnerability of the immune system during early development":
Serum Vaccine Antibody Concentrations in Children Exposed to Perfluorinated Compounds.
From this point on I will call this the "Antibody Paper."

The Breastfeeding Paper's authors used the same data from the same people used in the Antibody Paper.

The Breastfeeding Paper authors took from those 656 children studied this data:
During a 12-month period of the follow-up period, a subgroup of mothers was invited to bring in their children for an examination and blood tests at ages 11 months and 18 months
Remember this:
The prenatal exposure was assessed from the mother’s serum-PFAS concentrations at pregnancy week 32
The data in the Breastfeeding Paper came from 81 mothers of the cohort of 656 used in the Antibody Paper.

Can we agree that the Mother's serum PFAS concentration detected in the Antibody Paper are what is being used in the Breastfeeding Paper for month 0?  There was no additional analysis performed by the Breastfeeding Paper's authors.  The 81 mothers used in the Breastfeeding Paper were part of the 656 mothers used in the Antibody Paper.

I am pretty sure I am correct on this and I am not missing something or misreading their paper.

Here is where I started to have my doubts on the model's findings they reported.  I know better than to accept the conclusion of a paper without first looking at the data.  Statistics and squishy wording are used a lot in peer reviewed journal papers to support or elude to a finding of positive or negative outcomes.

With this in mind, what does their data say?

Let's look at Table 1 in the Breastfeeding Paper:

Source: Breastfeeding Paper
Let's look at the data for "0 month: aka: birth - in particular the serum concentrations for 80 mothers who had their serum concentrations for PFAS's measured at pregnancy week 32.

Source: Breastfeeding Paper - Excerpt from Table 1
We now need to agree that the serum concentration in Table 1 is in ng/mL.  Which means that for 80 mothers pulled from the 656 mothers used in the Antibody Paper, these 80 mothers had a geometric mean of 6.0 ng/mL of PFOS.

The authors of this paper - see note at bottom of Table 1 - use "median" for "geometric mean."  They are not the same, but that point is for another paper someone else can write about statistics.

What is important is that we agree that the Breastfeeding Paper authors are telling us that the geometric mean for PFOS in these 80 mothers was 6.0 ng/mL.

We need to also agree that the IQR reported - 5.2 and 7.2 - means that 75% of the PFOS concentrations found in these 80 mothers were no higher than 7.2 ng/mL

Source
 Still with me?

According to the Breastfeeding Paper's authors, the serum concentration for PFOS used in their model for each of the 80 mothers had a geometric mean of 6.0 ng/mL and an IQR of 5.2, 7.2 which means 75% of the PFOS found in these 80 mothers were below 7.2 ng/mL.

Those 80 mothers were pulled from the 656 mothers with serum concentrations of PFOS collected at week 32 of pregnancy in the Antibody Paper.

In order for me to be correct in what I am about to show, my observation of their data must show that a geometric mean of 6.0 ng/mL and an IQR of 5.2, 7.2 was used in their model that produced a result that allowed them to make this statement:
The duration of exclusive breastfeeding was associated with increases of most PFAS concentrations by up to 30% per month, with lower increases during partial breast-feeding.
Next post: Part 9

Saturday, September 12, 2015

Breast Milk and PFASs - Part 7

In their paper:
Breastfeeding as an Exposure Pathway for Perfluorinated Alkylates
The authors state:
Adverse effects of PFASs reported in children with similar serum-PFAS concentrations include immunotoxicity, as revealed by decreased antibody concentrations toward childhood vaccines and increased frequency of common infections.
and...
Our results show that four of the major PFASs tended to increase substantially during the breast-feeding period, thereby suggesting that human milk is a main source of exposure during infancy.
This is where the focus needs to be.  Should a new mom be concerned about this?  The news articles generated from the publication of this paper all screamed about toxic chemicals in breast milk and how they are passed on to your baby.

Here's the thing though.  This paper only looks at PFASs as a toxic chemical in breast milk. The concern therefore will only be for PFASs being present and passed on to the baby through breast feeding.  If they are present, the concern the authors tell us is because they could decrease antibody concentrations and increase the frequency of common infections.

If they are present...decrease antibodies for tetanus and diphtheria, and more common colds and gastroenteritis.

If they are present, that is what the author's of the paper contend could be the negative health outcomes.

If a new mom, because she read or was told about the news stories that resulted from this paper, chooses not to breastfeed because of this concern, then there will be zero benefits her baby receives.

Zero benefits if breastfeeding is not provided to the baby.

Zero benefits because of this paper.

The "toxic" chemical in the news stories is for PFASs.  The health concerns they tell us could result from an increase in exposure are decrease antibodies for tetanus and diphtheria, and more common colds and gastroenteritis.

What's your point Bowman?  You are beating a dead horse again.

Yeah...But that understanding is important here.  Are all mothers who want to breastfeed their baby going to put their baby at risk for decreased antibodies for tetanus and diphtheria, and more common colds and gastroenteritis.

Does this paper provide enough support for a new mother to give up breastfeeding to protect their baby from the harm of PFAS?

We can take the claim of an increase in common colds and gastroenteritis off the table of potential negative health outcomes.  It is not supported (see previous post).  This leaves the decrease in antibodies for tetanus and diphtheria.

The paper they cite; "Serum Vaccine Antibody Concentrations in Children Exposed to Perfluorinated Compounds," tells us this:
These results indicate that PFC exposures at commonly prevalent serum concentrations are associated with lower antibody responses to childhood immunizations and an increased risk of antibody concentrations below the level needed to provide long-term protection.
However...
The prenatal exposure level, as indicated by the mother’s serum concentration during pregnancy, was less clearly associated with the antibody outcomes.
That's important here.  What these guys say in their paper - the paper cited to support the negative health outcome of "decreased antibody concentrations toward childhood vaccines" - is that the mother's serum level of PFASs had a weak association with the antibody outcomes seen at 5 and 7 years.

So?

So if the mother's serum concentration during pregnancy is "less clearly associated with the antibody outcomes" then the adverse effects stated by the authors in their paper "Breastfeeding as an Exposure Pathway for Perfluorinated Alkylates" cannot support the negative health outcome of a decrease in antibodies for tetanus and diphtheria.

How can you say that Bowman?

Because these guys used the same cohort as the guys they cited.  Its the same data, the same serum concentrations, the same kids, the same mothers.

If the original paper "Serum Vaccine Antibody Concentrations in Children Exposed to Perfluorinated Compounds" tells us they found that "the mother’s serum concentration during pregnancy, was less clearly associated with the antibody outcomes" then the paper titled "Breastfeeding as an Exposure Pathway for Perfluorinated Alkylates" should not elude to negative health outcomes from breastfeeding and PFASs.

Here is what they state in the Breastfeeding paper:
Adverse effects of PFASs reported in children with similar serum-PFAS concentrations include immunotoxicity, as revealed by decreased antibody concentrations toward childhood vaccines and increased frequency of common infections.
That's in their paper.  This is too:
Given the importance of postnatal development of acquired immune function, the shape of the serum concentration profile may be important for PFAS-associated immune deficits.
Based on what? The guys they cited, the guys who provided the data they used, tell us this:
The prenatal exposure level, as indicated by the mother’s serum concentration during pregnancy, was less clearly associated with the antibody outcomes.
So if the prenatal exposure level in the mother is less clearly associated with the antibody outcomes, should a new mother forgo breastfeeding to decrease the risk of decreasing antibody outcomes?

No.  Why? Because the prenatal exposure level, as indicated by the mother’s serum concentration during pregnancy, was less clearly associated with the antibody outcomes.

But...that's the mother's serum exposure before the baby is born.  The paper tells us that "human milk is a main source of exposure during infancy."

Work with me here...

If a baby is exclusively breastfed for six months, then the major source of PFASs would be through the breast milk.  So the higher the serum concentration of PFAs before birth in the mother, the more PFASs transferred to the baby.

So...if  "the mother’s serum concentration during pregnancy, was less clearly associated with the antibody outcomes" at 5 and 7 years then breastfeeding, and it is the decrease in antibodies found at 5 and 7 years that supports this statement:
Adverse effects of PFASs reported in children with similar serum-PFAS concentrations include immunotoxicity, as revealed by decreased antibody concentrations toward childhood vaccines...
 Breastfeeding is therefore not shown to be contributing to an increased risk of antibody outcomes.

How can I state that when we are talking about breastfeeding and not the mother's serum concentration?

The authors of "Breastfeeding as an Exposure Pathway for Perfluorinated Alkylates" built a model using data from "Serum Vaccine Antibody Concentrations in Children Exposed to Perfluorinated Compounds"

This model, they contend, shows this:
The duration of exclusive breastfeeding was associated with increases of most PFAS concentrations by up to 30% per month, with lower increases during partial breast-feeding.
They then tells us this:
After cessation of breastfeeding, all serum concentrations decreased.
This is where we need to look at the data they used to make their model.  This mothers serum concentration becomes really important here.  This is where I had to pause and reflect when I read this:
As we used log scale transformations of PFAS concentrations, the higher milk concentrations from mothers with elevated serum concentrations were included in the model by default. However, neither the newborn baby’s PFAS concentrations nor the concentrations in milk were measured in this study, which instead relied on the maternal serum concentrations measured at a specified point during pregnancy.
Now, one more time...
The prenatal exposure level, as indicated by the mother’s serum concentration during pregnancy, was less clearly associated with the antibody outcomes.
Next post: Part 8

Wednesday, September 9, 2015

Breast Milk and PFASs - Part 6

In their paper "Breastfeeding as an Exposure Pathway for Perfluorinated Alkylates," the authors tell us that:
exposure via human milk could therefore lead to elevated serum concentrations in breastfed infants.
 This, they tell us, is a concern because:
Adverse effects of PFASs reported in children with similar serum-PFAS concentrations include immunotoxicity, as revealed by decreased antibody concentrations toward childhood vaccines and increased frequency of common infections.
I believe I showed in my previous post that there is nothing to support the "increased frequency of common infections."  This leaves us with the "decreased antibody concentrations toward childhood vaccines" concern.

The authors cite the paper called "Serum Vaccine Antibody Concentrations in Children Exposed to Perfluorinated Compounds"  In my last post I looked at this data, and ended the post with this:
Let's ignore that.  Let's assume that their negative numbers shown in Table 3 actually show that exposure results in a decrease of antibody concentration.  Let's forget about the values the model calculated with a 2-fold exposure, and just look at what they found.

Time out!

I write these posts in real time.  I start with a question and I try to answer it.  I am not sure if my thinking at the beginning will be changed at the end.  I am not sure what rabbit holes I will go down as I try to support my position.

This series of posts has been a challenge towards the end.  In my last post I looked at the data from the paper they cited to support the concern that:
...exposure via human milk could therefore lead to elevated serum concentrations in breastfed infants.
I am trying to support my position that breastfeeding in the first six months - based on WHOs recommendations - has better health outcomes for the baby then forgoing breastfeeding because "Breastfeeding can expose babies to toxic chemicals" as the news articles so quickly reported based on their paper's claim.

So it comes down to this:

Should a woman forgo breastfeeding based on this paper's contention that "exposure via human milk could therefore lead to elevated serum concentrations in breastfed infants?"
1. If that statement is true, it is true for one particular group of chemicals; PFASs.
and....
2. If there is elevated serum concentrations of PFASs in the baby who was breastfed, will those elevated levels of PFASs cause a negative health outcome?
and...
3. If those PFASs now in the baby will cause a negative health outcome for the baby, is that negative health outcome greater than the benefits of breastfeeding?
I am trying to understand what their data shows.  I am having a very difficult time understanding it.

Question 2 is the key to this.  Their paper claims that breastfeeding "could therefore lead to elevated serum concentrations."  This claim needs to be supported by data, and, if true, the elevated serum concentrations of PFASs must present a negative health outcome.

So here is where I am having trouble with this.  I need to know if PFASs are transmitted in breast milk, and if they are, is the baby impacted in a negative way greater than a baby who was not breastfed?

Which brings me to this point.  Their data does not make sense to me.  This is a a peer reviewed paper and has a "Harvard" affiliation.  All of this is making me question myself.  I must not be seeing this correctly.

I have read, reread, and re-reread, and re-re-reread these papers many times.  The more I read them the more convinced I am that I must be missing something or am too much a novice to understand them.

Surely they could not have left this information out intentionally or accidentally.  The peer review would have caught it.  Its not there, things are missing, graphs are not explained....am I really seeing what I think I am seeing or am I missing it because I am below some level of understanding needed to review this paper?

Then I remember that its not me that has to support their findings, its them.  Did they?

Next post: Part 7

Breast Milk and PFASs - Part 5

Let's look at the author's statement in their paper "Breastfeeding as an Exposure Pathway for Perfluorinated Alkylates":
a major concern [because] PFAS exposure may undermine childhood immunization programs.
Is it?  They cite two papers that make this claim:
  1. Pre-natal exposure to perfluoroalkyl substances may be associated with altered vaccine antibody levels and immune-related health outcomes in early childhood
  2. Serum Vaccine Antibody Concentrations in Children Exposed to Perfluorinated Compounds
Let's look at the first one.
Most clearly, a 2-fold increase in PFOS exposure was associated with a difference in [antidiphtheria] antibody concentration of -39% (95% CI, -55% to -17%) at age 5 years before the booster.
Thus, a 2-fold increase in PFOA exposure was associated with differences of -36% (95% CI, -52% to -14%) and -25% (95% CI, -43% to -2%) for tetanus and diphtheria, respectively.  
Okay...assuming that to be true, now we are looking at something that may be significant, not just statistically significant.

Why would this drop in antibody concentration be of a concern?
PFC exposures at commonly prevalent serum concentrations are associated with lower antibody responses to childhood immunizations and an increased risk of antibody concentrations below the level needed to provide long-term protection.
Okay...again, assuming their data does actually show a decrease, this is a concern.

What did the second paper show?
Based on the β -values, the strength of the association between rubella antibody-levels and PFAS concentrations were PFNA >PFOA >PFHxS >PFOS. No significant associations were found between the concentrations of PFAS and vaccine antibody levels to the other vaccines.
Though not in complete agreement, there is a case to be made that PFAS concentrations in serum blood impact antibody levels.

The first paper supports its findings stating:
Our findings are supported by several. though not all, experimental studies in rodents, in which adverse effects of PFOS on humoral immune function were observed at serum concentrations similar to those reported in the present study and at levels prevalent in the United States.
Why this lowered antibody levels might be considered a "major concern" is based on this:
An antibody concentration greater than 0.1 IU/mL is considered an important indicator of protection in accordance with the public health rationale for routine vaccinations. Prenatal and postnatal PFOS exposures, as well as postnatal PFOA exposure, were associated with increased odds of antibody concentrations below the protective level.
 Let's look at the data for the 1st paper cited.
Most clearly, a 2-fold increase in PFOS exposure was associated with a difference in [antidiphtheria] antibody concentration of -39% (95% CI, -55% to -17%) at age 5 years before the booster.
That's a result based on a model they generated:
Structural equation models were generated to determine the joint associations of PFCs with the overall antibody concentrations.
And those models were designed from the statistical data they calculated:
Multiple regression analyses with covariate adjustment showed that prenatal exposures to both PFOS and PFOA, as indicated by the maternal serum concentrations, were negatively associated with antidiphtheria antibody concentrations (TABLE 3)
 Let's look at Table 3:


See those 95% Confidence Intervals (CIa)? Here is what they show:
Confidence intervals provide an ‘estimate interval’, that is, a range of values around the point estimate within which the true value can be expected to fall.
In statistics, this statement is true:
The wider the confidence interval is, the more variability in the sample, and the less precise the point estimate.
The authors in the cited paper claim that "both PFOS and PFOA, as indicated by the maternal serum concentrations, were negatively associated with antidiphtheria antibody concentrations."

The CIs for these percent difference result range from a negative percentage to a positive percentage.


This means that although they report a negative number (a decrease in the percentage of antibodies when compared to a population that was not exposed), the true value falls between that range.  It could be any number between -31.9 and +18.7.

This range - from negative to positive - is seen in the majority of results in Table 3.  It appears that the authors ignored that. and focused on the mean value - a negative number - that the statistics program spat out.

This range, at least to me, makes the statement of a negative difference in antibody concentrations found, questionable.  Its too variable to say the mean is representative of the population at large.

Let's ignore that.  Let's assume that their negative numbers shown in Table 3 actually show that exposure results in a decrease of antibody concentration.  Let's forget about the values the model calculated with a 2-fold exposure, and just look at what they found.

Next Post" Part 6

Note: This was written earlier than post date.  My next post will explain why.

Saturday, September 5, 2015

Breast Milk and PFASs - Part 4


This fire,,,:


...was started from this paper...:


...that states the following...:
Concentrations of PFOS and PFOA in breast milk are generally between 20 and 100 ng/L,4 and a daily milk intake of about 125 mL/kg body weight5 could easily contribute about 6 ng/kg per day or a total of 1 μg/kg for the recommended 6 months of breast-feeding.
...which they say is a concern because...:
exposure via human milk could therefore lead to elevated serum concentrations in breastfed infants.
... and that it also is...:
a major concern [because] PFAS exposure may undermine childhood immunization programs.
...as well as...:
 increased frequency of common infections

...which then leads all the news organizations and advocates to conclude:




There is nothing to support the statement of "increased frequency of common infections,"  In my last post I went over this, so to summarize, the paper they cited - the one single paper - used data from a questionnaire to determine,,,:
how many episodes of the following diseases/complaints the child had experienced in the last 12 months: common colds and other upper respiratory tract infections (hereafter called common cold), otitis media, pneumonia, gastroenteritis with vomit or diarrhea, and urinary tract infection.
Only the common cold and gastroenteritis gave any kind of statistically significance and that was only for the number of episodes, which I think I showed in my last post was insignificant even though it was statistically significant.

I contend that the evidence presented does not show an "increased frequency of common infections" which means we can cross that off the list as to why "concentrations of PFOS and PFOA in breast milk" could be a "major concern."

This leaves "undermine childhood immunization programs" as a possible "major concern" as all they presented as evidence were two citations.
  1. Pre-natal exposure to perfluoroalkyl substances may be associated with altered vaccine antibody levels and immune-related health outcomes in early childhood
  2. Serum Vaccine Antibody Concentrations in Children Exposed to Perfluorinated Compounds 
Let's have a look shall we...

Next post: Part 5

Saturday, August 29, 2015

Breast Milk and PFASs - Part 3

The Mogenson paper "Breastfeeding as an Exposure Pathway for Perfluorinated Alkylates" that initiated the "Breast milk may be tainted with toxic chemicals" news articles on Google make this statement as to why PFASs are a possible concern if they are found in breast milk:
Adverse effects of PFASs reported in children with similar serum-PFAS concentrations include immunotoxicity, as revealed by decreased antibody concentrations toward childhood vaccines and increased frequency of common infections.
Let's look at their statement that PFASs result in an "increased frequency of common infections."

This is based on a single paper they cited titled:
Pre-natal exposure to perfluoroalkyl substances may be associated with altered vaccine antibody levels and immune-related health outcomes in early childhood.
 Here is what the author's of that cited paper conclude:
In the present study, PFAS concentrations were associated with reduced antibody levels to the rubella vaccine and increased number of episodes of common cold and gastroenteritis, suggesting that pre-natal exposure to various PFAS may lead to immunosuppression in early childhood.
Now I am not at all good with them there statistics these science papers use. I am, however, good enough to look stuff up and get a feel for what is going on with the data they report.  They say there are lies, damn lies, and statistics, and I agree.  I have read enough journal peer-reviewed papers to come away scratching my head as to how they can conclude what they do and put it in a paper for all the world to read.

The reason I am once again going on and on about a single topic is to provide support for why I think it has committed a wrong.  In this case, it is not that the data is wrong - it may or may not be - it is the simple fact that what they elude to - that "breastfeeding being an important exposure pathway to some PFASs in infants" sends the wrong message to the public and specifically mothers who want to do what is best for their baby.

Assuming that breast milk does increase the amount of PFASs in the baby, does that increase contribute to a negative health outcome?  The two papers they cite state that these compounds "may undermine childhood immunization programs" as well as "increased frequency of common infections."

Let's look at the evidence to support the "increased frequency of common infections."

According to the cited paper "Pre-natal exposure to perfluoroalkyl substances may be associated with..." the mothers in the study were asked in a questionnaire:
Concerning infectious diseases, the mothers were asked how many episodes of the following diseases/complaints the child had experienced in the last 12 months: common colds and other upper respiratory tract infections (hereafter called common cold), otitis media, pneumonia, gastroenteritis with vomit or diarrhea, and urinary tract infection.
The authors report:
When analyzing common cold for the third year of life as a binary variable (yes/no), no statistically significant associations were found (Table 5).
This means that there was no difference between the exposed group and the non-exposed group (the control) when asked the yes/no question on colds.

They then state:
With regard to infectious diseases, the maternal concentrations of PFOA and PFNA were positively-associated with the number of episodes of common cold for both the children’s third year of life and all 3 years merged. PFHxS was positively-associated with the children’s number of episodes of common cold for all 3 years merged in the bivariate analysis only (Table 5).
No statistically significant associations between perfluoroalkyl substances and the common cold,  otitis media, pneumonia, gastroenteritis with vomit or diarrhea, and urinary tract infection.

They state that they found that "increased concentrations of PFOA and PFNA were associated with increased number of episodes of common cold."

The statistical data they present in Table 5 resulted from:
Poisson regression analyses were used for health outcomes consisting of count data (number of episodes of common cold and and gastroenteritis),
Like I said earlier, I am not well versed in all things statistics.  So I went looking to see what the "β-value" in Table 5 means:


I went a Googeln' and found this helpful information:

Assuming I am understanding this correctly a higher  β-value supports the claim that "increased concentrations of PFOA and PFNA were associated with increased number of episodes of common cold."
With regard to infectious diseases, the maternal concentrations of PFOA and PFNA were positively-associated with the number of episodes of common cold for both the children’s third year of life and all 3 years merged. PFHxS was positively-associated with the children’s number of episodes of common cold for all 3 years merged in the bivariate analysis only (Table 5).
The question I have, when looking at Table 5's data for he common cold, is what does positively-associated actually represent here?

What the authors of this paper report is an increase that is statistically significant when the β-value had a p-value ≤ 0.05.



The data that gave them this statistically significance β-value in Table 5 that supports their claim of "positively-associated with the children’s number of episodes of common cold" comes from a questionnaire given to the mother.
At the age of 1, 2, and 3 years, a questionnaire was sent to the participants. ...Concerning infectious diseases, the mothers were asked how many episodes of the [common cold] the child had experienced in the last 12 months.
Yeah, these mom's may recall with 100% accuracy the number of colds their child got last year, and when you put all the numbers into the statistics computer program it spits out a β-value and a p-value, but does a p-value below 0.05 support anything other than the β-value being statistically significant?

Yippie!  I saved one dollar on my purchase of a new car!  That's a positive increase in my bank account!

If you look at the β-values associated with those p-values, they are not big numbers.  If you look at all the data on incidence of common colds reported by the moms, 50% showed no statistical significance.

The authors are not incorrect when they state "positively-associated with the children’s number of episodes of common cold" its just that the "positive" they are speaking about looks to be an insignificant increase.

When you add this to the fact that a questionnaire that asks a mom to recall the number of colds in the past year is fraught with bias and error, and you look at the very small number of participants, the support for the statement in the Mogensen paper on Breastfeeding that "adverse effects of PFASs reported in children with similar serum-PFAS concentrations include...increased frequency of common infections" should never have been made.

Do I need to show you the results for gastroenteritis or will you take my word for it that it paints the same picture as the common cold data in Table 5 did?

Statistically significant results should actually mean something other than they were statistically significant.

Next post: Part 4

Breast Milk and PFASs - Part 2

Let's look at their paper (sorry, its behind a paywall so I cannot link to it.):
Breastfeeding as an Exposure Pathway for Perfluorinated Alkylates
Why the big deal?  Why do the five authors believe that PFASs in breast milk is a potential concern?

If it is in breast milk, then there is uptake by the baby.  Now the baby has PFASs in their system.  What's so bad about that?
PFASs can have immunotoxic effects, and a major concern is that PFAS exposure may undermine childhood immunization programs.
and...
Due to the particular vulnerability of the immune system during early development, the sources of PFAS exposure in infants are of special interest.
That's why these guys think their study is important.  Because "PFAS exposure may undermine childhood immunization programs."

What is that based on?  They cite a paper called "Serum Vaccine Antibody Concentrations
in Children Exposed to Perfluorinated Compounds" (which is behind a paywall so I cannot link it).
Our findings are supported by several, though not all, experimental studies in rodents, in which adverse effects of PFOS on humoral immune function were observed at serum concentrations similar to those reported in the present study and at levels prevalent in the United States.
There were adverse effects on humoral immune function observed.
An antibody concentration greater than 0.1 IU/mL is considered an important indicator of protection in accordance with the public health rationale for routine vaccinations. Prenatal and postnatal PFOS exposures, as well as postnatal PFOA exposure, were associated with increased odds of antibody concentrations below the protective level. 
Exposure increased the odds of antibodies being below the protective level.
If the associations are causal, the clinical importance of our findings is therefore that PFC exposure may increase a child's risk for not being protected against diphtheria and tetanus, despite a full schedule of vaccinations. 
What they found was this:
Most clearly, a 2-fold increase in PFOS exposure was associated with a difference in antibody concentration of -39% (95% CI, -55% to -17%) at age 5 years before the booster.
I am not going to argue CIs or PFOSs or PFASs or whatever.  I am going to take their data as is.  A 2-fold increase in concentration decreased the antibody concentration for tetanus and diphtheria, (keep reading to see how this 2-fold issue came about)

This is where I separate from the five authors.  If they are basing their concern on this:
Adverse effects of PFASs reported in children with similar serum-PFAS concentrations include immunotoxicity, as revealed by decreased antibody concentrations toward childhood vaccines and increased frequency of common infections.
...then the benefits they attribute to WHO:
Breastfeeding is recommended by WHO as the exclusive food source for infants during the first 6 months after birth and onward partially with supplementary food up to age 2 years.
...must be less then the risk of a "decreased antibody concentrations toward childhood vaccines and increased frequency of common infections" for a mother to stop breastfeeding.

PFASs are a concern because of a "decreased antibody concentrations toward childhood vaccines and increased frequency of common infections" according to the papers authors.

Their paper generated this news article stating:
BREAST MILK IS BEST FOR BABIES BUT THE MOMS COULD ALSO BE PASSING HARMFUL CHEMICALS
See what you started?  Hopefully you can see where I am going with this and why it bothers me.  If one mother changes her mind about breastfeeding because she does not want to pass harmful chemicals to her baby, then the positive benefits of breastfeeding, as described by WHO, will not be received by that baby.  One risk is substituted for another risk. 

This means that there had better be a real risk of "decreased antibody concentrations toward childhood vaccines and increased frequency of common infections" when breast milk is given to the baby., and that risk is substantially decreased if the baby receives formula.

Then, if formula is used, the benefits not received from breastfeeding are negated by that decrease in risk of decreased antibody and frequency of common infections,

This makes me ask the question; how confident am I in the data they used to make the statement "decreased antibody concentrations toward childhood vaccines and increased frequency of common infections."

I am pretty confident in the data that WHO used to recommend breastfeeding.  There is a lot of it out there.  But for PFASs and PFOS there is not.  There seems to be a small group looking at into them and they seem to cite each other's papers.  That makes me a little skeptical in how "bad" they might be.

Now I am writing this, like I usually do, in real time.  That is, I do not have the data in front of me.  I write as I look it up.  I have no pre-formed conclusion on the validity of their findings and data.  I am concerned/agitated because I think they found all the attention on their work outweighed their concern that women may look at it and chose not to breastfeed, because, you know, these smart scientists, one from Harvard no less, found that breast milk could be exposing a baby to toxic chemicals.

There had better be some convincing data to justify the decision a women might make to not breastfeed based on this journal article and the news stories about it.


Next Post: Part 3

Breast Milk and PFASs - Part 1

This caught me a bit off guard on my Google News Feed:

Huh? soon gave way to no, no, no...please don't go there.  And that was without looking at the data to support that headline.

Having gone through a public health masters' program, you get indoctrinated into the concept of the of "the greater good."  You learn that there is a risk of a negative health outcome with almost everything you do, drink, eat, breath, or come in contact with.  You decide based on what gives you the best outcome overall.  And you decide based on compelling evidence to do, or to do not.

I am a chemical hazard guy.  A hazardous waste guy to be specific.  I like looking at chemicals and their risk.  I buy into the notion that there are positive health outcomes when you decrease the amount (dose) of the chemical.  I also accept that there is a dose you - including a baby - can be exposed to where there is minimal risk of a negative outcome.

I also accept, advocate, and believe to be true the "Donnelly Risk Paradigm" which you can read about here.  Basically, if there is exposure, there needs to be uptake and there needs to be a negative health impact.  Without exposure there is no uptake, without uptake there is no negative health impact.  The problem here is, that even if there is exposure and uptake there does not necessarily manifest a negative health outcome since the body is pretty good at detoxifying stuff that gets into it.

Limiting exposure is a good thing but exposure and uptake does not mean a bad thing will happen (see the liver).

With this in mind, let's look at the paper that got Google to tell the world about breast feeding giving your baby toxic chemicals.
Philippe Grandjean, the study author and environmental health expert at Harvard T.H. Chan School of Public Health stated that it was indeed an absurd situation breastfeeding women need to think of the kind of chemical exposures they could contribute to the child although breast milk is heralded as the best possible source of nutrition for the baby.
Wait...Harvard...no, no, no...Will this journal paper discourage a new mom from breastfeeding her baby?  Was that considered before they published it?  One news article goes on to quote one of the authors on this:
Grandjean and the other experts continue to emphasize that breast milk still is the best food for babies. But, it is just that it is less healthy and pure than was intended by nature and previously believed.
That's real helpful there professor.  What the public now sees is "Breastfeeding can expose babies to toxic chemicals."

Arggg.

Remember, the greater good!  Breastfeeding is for the greater good of the baby.  If you are going to tell new mothers that their breast milk is "less healthy and pure" then you should have anticipated it going full speed ahead to "breast milk may be tainted with toxic chemicals" once the press got a hold of it.  You and your cohorts on this paper should have understood this, so your research better show that breast milk is contaminated high enough so that continued feeding is more harmful to the baby then the benefits.

Before I go on, please note that I am all for this type of research.  It is important to understand exposure pathways.  If PFASs are causing harm, then this type of research is important.  But you need to chose your words carefully and keep this research on the down-low, because all the public sees is "Breastfeeding can expose babies to toxic chemicals."

And armed with that Google news feed title, can you blame a new mother for choosing not to breastfeed?

Next post: Part 2

Sunday, August 9, 2015

Oops! EPA Accidentally Pollutes the Animas River

Edit: March 18, 2016: BOI Report on the incident. 

Rivers are not supposed to look like this.

Source
Update video on the spill.

For those readers who may be looking at the news, and the recently posted lab data, maybe I can help make some sense out of those numbers.

I am a public health guy.  I love fish and plants as much as anyone else, but I really don't deal with aquatic toxicity.  So looking at the lab results, I see a lot of "metals" that are not the toxic metals to human health I deal with,

By the way...Ignore all the letters by the results.  Those are important, but, for all intents and purposes, the values reported are the values we can assume were actually present at the time the sample was taken.  D, for example means they had to dilute the sample to get it low enough for the instrument to read it without overloading it.  Too much and the instrument's reading goes off the scale, so you dilute it, and then take the result and estimate how much is in there.  There is error put into that result when it is denoted with a "D", but again, these results are so high that potential error is meaningless.

Let's look at sodium for example.  The lab reports a maximum concentration of 11,100 ug/L at the the 32nd St Bridge.

That's 1,110 parts per million, ug/L is ppb, there are 1000 ppb in one ppm.

So I asked myself, 'what is the normal sodium concentration found in freshwater streams?'

Good ol' Google...Sodium looks to be about 5 ppm as a high concentration.  So the sodium is elevated for sure, but less than sea water (10,500 ppm).

Now let's look at the human health concerns.  Assuming there is no cyanide, the primary concern for this water coming from a mine is the heavy metals, and for those, I want to look at just what we call the "RCRA 8."

Looking at the analytical results, it looks like only lead is a really big concern - human health wise.

Source
Let's look at two of the metals.  The others are important, but these two have the highest concentrations and are a bigger deal toxicity wise.

Arsenic looks to be about 1080 at the highest concentration found.  As you can see above, the MCL - U.S. EPA's drinking water standard - is 10 ug/L.  Now remember, that's for drinking the water.  And not just drinking it once, but drinking two liters per day, almost every day, for 70 years.  Drinking a glass of this water would not, based on the lab results shown, be a concern (it would probably taste terrible though).  Potable and Palatable!

Lead...on the other hand...well...

25,600 ug/L at sample location "A72."

The MCL for lead is 15 ug/L

That's 25 ppm of lead in that sample.  See the TCLP results above for lead?  5 mg/L or 5 ppm..

That water, from location A72,  meets the definition of a hazardous waste,  Not that that makes it "toxic", it just shows that the concentration of lead is pretty gosh darn high.

So...dilution will be the solution to pollution here, but this river was heavily contaminated by some toxic stuff, that should have never gotten into this river (call me Captain Obvious).

It will be interesting to see what takes place to the environment as this water makes its way downstream.

Time will tell.

Sunday, March 8, 2015

Bottle of Wine.... Gallo Glass vs. DTSC - Part 12

I'm not sure how Gallo Glass manages the EP sludge at their facility.  All I have to go on is the DTSC complaint, and that is heavily biased towards the findings the DTSC claims.

In the complaint, the DTSC acknowledges that HSC 25142.2 is in play:


The DTSC then bolsters its position on recycling with this:


It appears to me, that the DTSC takes issue with putting the EP sludge back into the process.  Why? is anyone's guess here.  Perhaps the arsenic, cadmium, lead, and selenium above TCLP thresholds gives them concern.  Though they state in their press release that they have "no evidence that consuming wine stored in these bottles poses a health threat," the thought of putting that stuff - that waste that would be hazardous waste - into wine bottles could be seen as off-putting.

However, if I understand the process Gallo Glass is using, what goes into the EP air pollution control device comes from the raw materials used to make the bottles.  In other words, those four metals are in the raw product that creates the EP sludge.  Unless the EP sludge is produced from a separate process where those metals are added, the EP sludge would - to me - have the same characteristics as the raw material.

What's important here, if a public health concern, or from DTSC's position, the protection of public health, is what leaches out of the bottles that are made with the EP sludge as an ingredient.  I would guess that this has been looked at.  The last thing any wine maker would want is to have their product meet the definition of a hazardous waste because it sat in a glass bottle.

Looking at this complaint objectively, it seems the DTSC is unsure of this, though they have had plenty of time to TCLP the wine bottles to see if the EP sludge is impacting the wine that is consumed.  Based on their press release, I am guessing that they did sample the glass as they claim they "have no evidence that consuming wine stored in these bottles poses a health threat."

Why the DTSC went after Gallo Glass regarding this process with such gusto seems very heavy-handed.  I can find no reason to view the addition of the EP sludge back into the process as anything other than a bona fide recycling process. I can see nothing in the complaint that leads me to see this as "sham recycling." Perhaps Gallo Glass failed to do this in the first place, or failed to respond in a forthright way.

I think the DTSC will not come out a winner on the claim of "surrogate disposal."  They probably will get Gallo Glass on the technicality of  HSC 25143.9 which states a "recyclable material shall not be excluded from classification as a waste ...unless all of the following requirements are met."

The complaint does provide documentation that EP sludge was not adequately contained.  They did get them for daily inspection, signage, employee training, secondary containment, contingency plan, and for failing to obtain a written assessment  EP sludge silo tank and its associated ancillary equipment and containment system.  They have to do that as part of HSC 25143.9.

What I did read in number 35 was "The EP sludge that did not make it into the silo or furnace was either unlawfully released into the environment or disposed of as a hazardous waste to an authorized landfill. The only issue here is "unlawfully released into the environment" as the furnace is recycling and the landfill is the only legal disposal option for EP sludge not recycled.

The complaint also states:


This may seem a little trivial, but the exemption is only for EP sludge that is recycled.  If it is not recycled, it must be managed as a hazardous waste.  So this "into the environment" they noticed becomes a big deal for that particular EP sludge.  Remember, in California HSC 25143.9 has specific management requirements in order to get exclusion.

So there you have it.  12 posts later and I am done making sausage. I know I said I would talk about the used oil issue, but I changed my mind.  It took me 12 posts just to discuss the recycling requirement for the EP sludge

Bottom line.  DTSC is wrong on the surrogate disposal claim and Gallo Glass needs to get their house in order and manage the EP sludge as if it is a hazardous waste.  That solid waste exclusion goes away real easy if you fail to recycle or manage it correctly.

Thanks for reading if you got this far.  I hope it helps you understand the complexity of a simple activity such as recycling.

End