What is Kipp doing to protect its workers from vapor intrusion? They won’t say.

Photo: Workers in Madison-Kipp factory.

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Kipp says they stopped using the highly toxic solvent tetrachloroethylene, also called perchloroethylene or PCE—the toxic chemical that was the main focus of the citizen class action lawsuit settled in 2013 (see more details about the lawsuit here and here).

However, in addition to PCE, Kipp also used the even more toxic solvent trichloroethylene, or TCE. TCE is a carcinogen and can cause neurological, immune, kidney, liver, reproductive, and developmental effects. It can also cause cardiac defects in fetuses whose mothers are exposed for even very short periods of time during pregnancy. See links to more information below

Did Kipp ever stop using TCE? What solvents is the company using now? How is Kipp protecting its factory workers from exposures to solvents used in the factory—and to PCE, TCE and other volatile organic chemicals (VOCs) seeping into factory air from the huge VOC plume below it? Sadly, this is just one of the many health and safety risks faced by Kipp’s workers, many of whom are minorities—see past stories here and here.

Last week, I sent the message below to John Hausbeck at Public Health Madison Dane County and Kipp’s environmental health and safety manager, Alina Satkoski. I have received no response.

Given this lack of response, I am assuming that Kipp is still using TCE—and is doing very little or nothing to monitor and protect its workers from exposures to the many volatile organic chemicals seeping into the factory from below. If Kipp is not using TCE anymore—and has been monitoring and protecting its workers from VOC exposures—why wouldn’t their health and safety manager say so right away?

Below–email message sent to Public Health Madison Dane County and Kipp environmental health and safety manager, Alina Satkoski:

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 screening levels 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.  Below my name, I pasted a summary from an EPA TCE risk assessment document re TCE and heart defects. You can find the IRIS info on TCE toxicity here and here.

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.

Thank you,

Maria

**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).