Kipp CEO refuses to answer questions about how company is addressing risks to factory workers
This is a followup to a previous post.
A month ago I emailed John Hausbeck at Public Health Madison Dane County for help answering a set of questions about Kipp factory workers’ exposures to volatile organic chemicals (VOCs)—especially trichloroethylene (TCE), which is more toxic than perchloroethylene (PCE). I copied Kipp’s Health & Safety Coordinator, Alina Satkoski. My original email is included in the previous post, and below. For more information about TCE’s toxicity, see my original email below and here.
The questions I asked? 1. What has been done to assess VOC levels in the Kipp factory? 2. What is being done to protect workers from exposures to these chemicals? 3. Does Kipp still use TCE? If they stopped using it, when did they stop? 4. What solvents does Kipp use now?
After about a month, I received no answer from Mr. Hausbeck or Ms. Satkoski.
I asked again, and on October 16, Alder Rummel followed up, asking Ms. Satkoski to address the questions. Satkoski answered that they had assessed vapor intrusion in the office portion of the plant in 2014. I reminded Ms. Satkoski that I had asked about exposures to the factory workers—not just the office workers.
At this point, Kipp CEO Tony Koblinski inserted himself into the email chain. He refused to answer the questions I posed. He accused me of “twisting the truth” and said he is “done with me” but I can “write whatever the hell I want.” The full email chain is below. The response I emailed him is here.
Given Mr. Koblinski’s evasion of the questions, it seems logical to conclude that: Kipp has not assessed VOCs in the factory or VI risks to factory workers (only office workers); Kipp is not doing anything to protect factory workers from exposures to VOCs/vapor intrusion; Kipp still uses TCE and; Kipp is not willing to tell elected officials, the public health department, and the public what solvents it uses currently.
If Kipp has assessed vapor intrusion risks to its factory workers, wouldn’t it be to their benefit to say so? Similarly, if Kipp was no longer using TCE, would they want to tell us that? If Kipp is willing to share a list of the solvents they currently use—and has nothing to hide—why haven’t they done so?
Chain of emails (most recent first):
On 10/18/2016 6:07 PM, Tony Koblinski wrote:
You are wrong.
Again, what a truly strange distribution list I find myself in.
This, I assure you, is the last time that I (or any of my staff) will respond directly to you, as your motives have baffled me since the day I met you.
Concern for our workers safety and well-being is the highest priority we have here at Kipp. Our actions to safeguard our team result in benchmark safety and workers compensation rates.
I (like all small business owners) have plenty of regulatory oversight and I don’t feel a need to satisfy your curiosities.
You have already demonstrated to me your keen ability to twist the truth and distort the facts and frankly, I’m done with you. (I think the exact moment was when you tried to give people the impression that Kipp was responsible for the tragic death of one of our long time employees who died of heart failure).
So, if you want to continue to play investigative reporter, have at it, but Kipp is not talking directly to you or cooperating in any way.
You continue to publish whatever the hell you want, and I will continue to run this business lawfully, responsibility and strive to continue to be a positive force in the surrounding community.
On Tue, Oct 18, 2016 at 2:51 PM, Maria Powell (MEJO) <email@example.com> wrote:
To be clear, your unwillingness to answer my questions indicates that:
-Kipp has not assessed VOCs in the factory or VI risks to factory workers (only office workers).
-Kipp is not doing anything to protect factory workers from exposures to VOCs/vapor intrusion.
-Kipp still uses TCE.
-Kipp is not willing to tell elected officials, the public health department, and the public what solvents it uses currently.
If I am wrong, please do correct me.
On 10/18/2016 2:29 PM, Tony Koblinski wrote:
I am going to respectfully put an end to this email string.
The WDNR (as well as the EPA) have actively directed a comprehensive investigation of this site over the last several years.
We have spent millions of dollars testing and remediating the site with their oversight.
All pertinent information to the investigation is part of public record.
On Tue, Oct 18, 2016 at 1:25 PM, Maria Powell (MEJO) <firstname.lastname@example.org> wrote:
I already have the indoor office results and have had them for years. They indicate there could be problems, but there weren’t enough tests to really say.
However, to be clear, I didn’t ask about assessments in the office portions of Kipp. I asked about how vapor intrusion risks related to VOCs,** but especially TCE, were assessed in the factory portion of the plant.
I also asked some other questions. Here are the questions I asked–copied from below:
1. What has been done to assess VOC levels in the Kipp factory? 2. What is being done to protect workers from exposures to these chemicals? 3. Does Kipp still use TCE? If they stopped using it, when did they stop? 4. What solvents does Kipp use now?
I hope you can answer them as soon as possible.
**To be clear “VOCs” include PCE and its breakdown products (TCE, DCE, VC) as well as a number of other volatile chemicals that are known to be under the Kipp factory in soils and groundwater.
On 10/18/2016 7:36 AM, Alina Satkoski wrote:
We have completed indoor air sampling for TCE and other VOCs. This work was completed in 2013 and 2014 and the work is summarized in a Summary of Office Indoor Air Sampling Activities (February 2014) the MKC 2014 annual report. These reports are publicly available through the DNR’s website.
On Sun, Oct 16, 2016 at 7:57 PM, Rummel, Marsha <email@example.com> wrote:
Can you help provide answers?
From: Maria Powell (MEJO) <firstname.lastname@example.org> Sent: Thursday, October 13, 2016 10:07 AM To: Hausbeck, John Cc: Rummel, Marsha; Rep.Taylor@legis.wisconsin.gov; Alina Satkoski Subject: Re: Assessing risks to Kipp workers?
Hello John (and Alina): Attached is a 2014 EPA memo supporting what I said below. I am still awaiting your response to my questions. Thank you, Maria
On 9/19/2016 2:36 PM, Maria Powell (MEJO) wrote:
John: I and other community members are still concerned about chemical exposures to all Kipp factory workers, especially women who are or could become pregnant. As far as VOCs and exposures via vapor intrusion, TCE is of particular concern because it is more toxic than PCE–it is a carcinogen and also causes neurological, immune system, kidney, liver, reproductive, and developmental effects. Many of the effects from fetal exposures may not show up until adulthood. Vapor intrusion RCLs for TCE are much lower than for PCE–see here.** Also, recently government risk assessors concluded that the weight of evidence indicates that TCE and/or its metabolites could cause cardiac defects in fetuses even if maternal exposure durations are short, one-time, and relatively low dose.
We know Kipp used TCE as well as PCE at least into the 1980s. There are still high levels of it under the factory, along with many other toxic VOCs. PCE, of course, breaks down to TCE–so there is an endless source under the factory and in the plume beneath the larger neighborhood.
In light of the above, can you help us find out: 1. What has been done to assess VOC levels in the Kipp factory? 2. What is being done to protect workers from exposures to these chemicals? 3. Does Kipp still use TCE? If they stopped using it, when did they stop? 4. What solvents does Kipp use now? I copied Alina, since she certainly must know the answers to these questions.
**Workplace standards for PCE and TCE are thought by experts to be very inadequate and unprotective of workers’ health based on the science. Even Henry Nehls-Lowe agreed with this.
The below text is from EPA’s “TSCA Work Plan Chemical Risk Assessment,” EPA Document# 740‐R1‐4002, Environmental Protection Agency June 2014, Office of Chemical Safety and Pollution Prevention–see here.
2.7 HUMAN HEALTH RISK CHARACTERIZATION (I highlighted key sentence) TCE and its metabolites are associated with adverse effects on cardiac development based on a weight‐of‐evidence analysis of developmental studies from rats, humans and chickens. These adverse cardiac effects are deemed important for acute and chronic risk estimation for the scenarios and populations addressed in this risk assessment. The rationale for using TCE associated fetal cardiovascular lesions for acute scenario is based on the relatively short critical window of vulnerability in humans, rodent and avian cardiac development.The rationale for using fetal cardiac effects for chronic risks estimation is also based on the fact that relatively low dose short term/acute exposures can result on long‐term adverse consequences on cardiac development persisting into adulthood. ‐‐
Summary of Weight‐of‐Evidence Analysis for Congenital Heart Defects
TCE exposure has been associated with cardiac malformations in chick embryos studies (Boyer et al., 2000; Bross et al., 1983; Drake, V. et al., 2006; Drake, V. J. et al., 2006; Loeber et al., 1988; Mishima et al., 2006; Rufer et al., 2008) and oral developmental toxicity studies in rats (Dawson et al., 1990, 1993; Johnson et al., 2005; Johnson, 2014; Johnson et al., 2003). In addition to the consistency of the cardiac findings across different species, the incidence of congenital cardiac malformation has been duplicated in several studies from the same laboratory group and has been shown to be TCE‐related (EPA, 2011e). TCE metabolites have also induced cardiac defects in developmental oral toxicity studies (Epstein et al., 1992; Johnson et al., 1998a, 1998b; Smith et al., 1989, 1992). For example, the Johnson et al. and Smith et al. studies reported increased incidences of cardiac malformation following gestational TCA exposures (Johnson et al., 1998a, 1998b; Smith et al., 1989). Similarly, pregnant rats exhibited increased incidence of cardiac defects following DCA exposure during pregnancy (Epstein et al., 1992; Smith et al., 1992).
A number of studies have been conducted to elucidate the mode of action for TCE‐related cardiac teratogenicity. During early cardiac morphogenesis, outflow tract and atrioventricular endothelial cells differentiate into mesenchymal cells (EPA, 2011e). These mesenchymal cells have characteristics of smooth muscle‐like myofibroblasts and form endocardial cushion tissue, which is the primordia of septa and valves in the adult heart (EPA, 2011e). Many of the cardiac defects observed in humans and laboratory species involved septal and valvular structures (EPA, 2011e). Thus, a major research area has focused on the disruptions in cardiac valve formation in avian in ovo and in vitro studies following TCE treatment. These mechanistic studies have revealed TCE’s ability to alter the endothelial cushion development, which could be a possible mode of action underlying the cardiac defects involving septal and valvular morphogenesis in rodents and chickens (EPA, 2011e). These mechanistic data provide support to the plausibility of TCE‐related cardiac effects in humans (EPA, 2011e).
Other modes of actions may also be involved in the induction of cardiac malformation following TCE exposure. For example, studies have reported TCE‐related alterations in cellular Ca2+ fluxes during cardiac development (Caldwell et al., 2008; Collier et al., 2003; Selmin et al., 2008).
Environmental and Safety Coordinator