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Public Health Madison Dane County

Madison polluter doesn’t like what he reads

Madison polluter doesn’t like what he reads

Graphic from the Nov 2, 2017  Isthmus weekly newspaper

The Wisconsin State Journal published an October 28, 2017 article, “Best estimate is plume from Madison-Kipp plant could reach drinking water in 5 years,” that earned a spirited response from Madison-Kipp Corp. CEO Tony Koblinski in his open letter to the newspaper.

“Why is there a seemingly renewed effort by you and the paper to cast Madison-Kipp as a public enemy…?” — Tony Koblinski, industrialist

“Journalism is printing what someone else does not want printed; everything else is public relations.” — George Orwell, visionary author

Here is MEJO’s response to Koblinski’s letter.

 

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Kipp CEO refuses to answer questions about how company is addressing risks to factory workers

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:

Ms. Powell.

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) <mariapowell@mejo.us> wrote:

Mr. Koblinski:

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.

Thanks! Maria

On 10/18/2016 2:29 PM, Tony Koblinski wrote:

All-

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.

Tony Koblinski

On Tue, Oct 18, 2016 at 1:25 PM, Maria Powell (MEJO) <mariapowell@mejo.us> wrote:

Hello:

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.

Thanks,

Maria

**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:

Hi Marsha,

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.

Thanks,

Alina

On Sun, Oct 16, 2016 at 7:57 PM, Rummel, Marsha <district6@cityofmadison.com> wrote:

Alina-

Can you help provide answers?

Thanks-

Marsha

From: Maria Powell (MEJO) <mariapowell@mejo.us> 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. 

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).

Alina Satkoski

Environmental and Safety Coordinator

Madison-Kipp Corporation

asatkoski@madison-kipp.com

Office: 608-242-5200

Cell: 518-265-7183

 

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

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

Photo: Workers in Madison-Kipp factory.

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:

Subject: Assessing risks to Kipp workers?
Date: Mon, 19 Sep 2016 14:36:25 -0500
From: Maria Powell (MEJO) <mariapowell@mejo.us>
To: JHausbeck@publichealthmdc.com <JHausbeck@publichealthmdc.com>
CC: Rummel, Marsha <district6@cityofmadison.com>, Rep.Taylor@legis.wisconsin.gov <rep.taylor@legis.wisconsin.gov>, Alina Satkoski <asatkoski@madison-kipp.com>

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# 740R14002, 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 longterm adverse consequences on cardiac development persisting into adulthood.

‐‐ Summary of WeightofEvidence 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).

 

 

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Why “safe” levels of toxic chemicals may not be safe

Why “safe” levels of toxic chemicals may not be safe

“There’s no problem; toxic exposure is too low to cause any harm” is a common response by pubic officials when citizens raise concerns about toxins in the environment, such a PCBs or atrazine.

MEJO board member Kristine Mattis explains why this assurance may not be accurate in this article published at Counterpunch Online:

Toxic Curve Ball: Why Outdated Assumptions to Determine “Safe Levels” of To…

By now, a large number of consumers are aware of the hazards of the synthetic compound bisphenol-A (BPA). Effect… [MORE]

 

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Is the City of Madison Following Its Pesticide Policies?

Is the City of Madison Following Its Pesticide Policies?

While in Warner Park on September 8 2014, I saw a Madison Parks employee spraying Roundup[1] near the Warner Park Community Recreation Center (WPCRC), including along sidewalks just a few feet from the center’s bike racks, where many people, including young children, walk, bike, and play. It was a breezy day.[2]

A few hours later, biking through the park again on my way home, I didn’t see any standard warning signs. Two days later, walking through the park, I noticed one sign, under some shrubs, near a raingarden in a corner of the parking lot hundreds of feet from the center’s entrance and bike racks where I had seen Roundup applied two days earlier.[3] It was not at all “readily visible,” as required by the policy. The raingarden was fenced off, and it appeared as if plants in the raingarden were sprayed (presumably to eradicate non-native and/or invasive plants).[4] I walked around the raingarden and saw no other signs.

Madison’s Pesticide Policies

Citizens in many U.S. cities, including New York City, have questioned the use of Roundup and other pesticides in parks and other public places because of growing evidence of their toxic effects on animals, plants, and insects, which can lead to cascading effects on whole ecosystems over the long-term, and the health risks they pose to pets and people (e.g., see herehere, here and here and many more…).

Since at least 1991, Madison citizens have advocated for –and elected officials have passed—various policies restricting pesticides in the city. Unfortunately, it seems that these policies are being ignored, are not enforced, and/or are perhaps “forgotten” over time.

In 1991, the Madison Common Council passed Resolution 47.702, which called for limits on the use of pesticides in Madison.[5] In 2002, citizens raised concerns about the rising use of Roundup in city parks, after which Mayor Bauman issued a moratorium on its use and directed several city committees to review the use and safety of Roundup.

We haven’t yet located records of exactly what these committees decided, but presumably their reviews led to the development of the city’s Integrated Pest Management (IPM) policy in 2004. That year, the Public Health Commission also recommended the formation of a “subcommittee of pesticide experts that could assist staff with the evaluation of plans and pesticide use reports.” This subcommittee was directed, per Madison General Ordinance (MGO) 7.01(1)(a), to meet every year to review agencies pesticide use reports to see how well they complied with the city’s IPM policy and submit these reports to the Board of Health.

It appears that the IPM policy developed in 2004 is still Madison’s current pesticide policy (though the subcommittee was recently dissolved—see below). The purpose of this policy is described as follows:

“The purpose of this policy is to eliminate or reduce pesticide use to the greatest possible extent. The City of Madison agrees with the US EPA that “all pesticides are toxic to some degree, and the commonplace, widespread use of pesticides is both a major environmental problem and a public health issue.” For this reason, all departments will evaluate and give preference to non-pesticide management practices and use reasonably available alternative pest control methods, will minimize their pesticide use through Integrated Pest Management, and will use least risky pesticides as a last resort.” (highlights added).

Further elaborating on the conditions in which pesticides may be used (as a last resort), the document notes, “Chemical pesticide may be considered if: a. The non-toxic methods of pest control, such as Cultural Controls, Physical Controls, Mechanical Controls, and Biological Controls have been shown to be ineffective; And; b. Monitoring has indicated that the pest will cause unacceptable health or safety hazards, or an unacceptable reduction in the intended use of the property.”

Will the small plants growing on the edge of the Warner Park parking lots cause “unacceptable health or safety hazards or an unacceptable reduction in the intended use of the property”? It’s hard to imagine how they would do so. Our guess is that these Roundup applications were done for aesthetic reasons, which is not in line with an IPM approach.

Did Parks staff consider and/or try alternative methods to eradicate the harmless vegetation before resorting to Roundup? Parks staff and volunteers did use alternatives in the past. According to the 2009 IPM report for the Madison Parks Department (see bottom of pg. 17) in 2009 an organic herbicide called Ground Force (made of citric acid, garlic extract vinegar and yucca extract) was used for weeds in the WPCRC parking lot. No synthetic pesticides were used on the WPCRC property at all. What organic alternatives, or other types of strategies, were tried this year before resorting to Roundup?

Regardless of Parks’ rationale for using Roundup in this context, if it was following IPM policy, the non-chemical alternatives that were attempted before resorting to Roundup, and the success/failure of these attempts, should have been recorded. Moreover, the amounts and types of pesticides used in the recent treatment—as well as the amounts of types of all pesticides used during 2014 (to date) in Warner Park and previous years—would be recorded.[6] Were they?

Pesticide Policy Committee eliminated in 2013

It’s not clear how well city agencies are following IPM policies currently, especially since the ongoing oversight process established 2004 is no longer in place. In May 2013, Mayor Soglin and Public Health Madison Dane County decided to eliminate the Pesticide Policy Committee, repealing MGO 7.01(1)(a). A May 30 2013 PHMDC document explains the reason for eliminating the committee:

“The Pesticide Management Advisory Subcommittee has been a great help to the Board of Health and PHMDC staff. With the subcommittee’s help, most City of Madison agencies have become more adept at applying integrated pest management (IPM) principles and have sought out pesticide professionals that support these principles.”

After highlighting this apparent success in implementing IPM, however, the document goes on to hint at problems assuring that all agencies complied with the policy, in part because the subcommittee had little power: “However, PHMDC staff and subcommittee members have been frustrated at times when City agencies have not made changes or improvements identified in the annual reports. The current policy places the responsibility for change on the board, committee, or commission that has oversight over the agency in question (Paragraph 5d). If this body does not support change in the agencies practice based on recommendations of the subcommittee, neither PHMDC nor the subcommittee have authority to pursue further action to ensure compliance.”

Recent documents indicate that the pesticide policy is still in effect despite the dissolution of the committee. The Pesticide Management Report for 2012-2013 states the following:

“…Reduction of pesticide use is important because misuse or overuse of pesticides is both an environmental problem and a public health issue…The Policy on Pesticide Use on City Property will remain in effect and Departments will be required to submit annual use reports/plans to Health, but review of the reports will be internal within Health.  The plan for the future will be a more informal review and to make the reports available for public comment/review, most likely online….While not perfect, it was felt that the majority of City Agencies have adopted IPM principles and practices since the Policy was implemented in 2004, and formal oversight by the committee was not needed.  Also factoring, was the difficulty in maintaining a full committee in recent years.” (underlining added)

If most agencies “have adopted IPM principles and practices” and “formal oversight by the committee” is “not needed,” then PHMDC should have detailed reports of their pesticide uses and amounts for 2014 and previous years, as well as alternatives attempted. We located only one fairly thorough report online from Parks for 2009 (linked to above), but no others. For other departments and years since 2004, we were only able obtain electronic copies of “Pesticide Management Reports.” These reports are not available to the public online as far as we can tell.

Further, the “Pesticide Management Reports” are not IPM reports; they are very brief summaries by PHMDC staff that do not include any pesticide use details. For instance, the 2012-2013 Pesticide Management Report (linked to above), which is similar to all the other reports, simply states “yes” under compliance for the Parks Division, and under “Successes and Commendations” it says “Good use volunteer efforts in non-chemical control.” Under “Concerns,” it says “none.” In 2014, as we recently witnessed, Parks decided that Roundup should be used around Warner Park Center parking lots and raingardens and it is not clear whether non-chemical controls were attempted. We would like to know what the rationale was for these applications, what alternative were considered, what quantities of pesticides were used, and where they were applied.

In sum, if IPM is indeed being followed by City of Madison agencies, then reports with specific IPM details should be available to the public online, with opportunities for the public to comment and provide input on them–the “plan for the future” stated by PHMDC in the 2012-2013 document cited above. At this point we are not aware of online IPM reports or opportunities for citizen comments.

We look forward to online, detailed IPM reports for City of Madison agencies, as well as opportunities to provide comments and input on them. Hopefully this plan will be implemented soon.

 

[1] The applicator told me what she was spraying.

[2]The pesticide applicator was wearing shorts, a short-sleeved shirt, and no protective gear (not even gloves). This seems inadequate to protect the applicator from dermal, eye, and/or inhalation exposures from pesticide spills or aerial drift. Typical guidelines usually wear latex/rubber gloves, protective eyewear, long pants, long-sleeved shirts, etc.

[3]According to Madison’s IPM policy, “A standard notification plan that provides, at a minimum, readily visible posting for a period of 24 hours prior to a pesticide application (when possible) and a minimum of 48 hours following the application. These time intervals may be extended based on health or safety concerns. For areas that receive pesticide applications on a regular basis, permanent signs will be posted.”

[4]Raingardens are created to facilitate the infiltration of water downward to groundwater—in part, to prevent potentially harmful runoff from going into surface water. It is a good thing to keep pesticides from running off into surface water, but if pesticides are sprayed on raingarden plants (native or not), they and/or their breakdown products (often just as if not more toxic than the active pesticidal ingredients) may filter down into groundwater. This is a troubling tradeoff. What quantities of pesticides were sprayed on this raingarden? What alternatives were attempted?

[5]The details of this policy are uncertain. Some newspaper articles give the impression it restricted pesticide use in the entire city, and others suggest it restricted use only on Madison Metropolitan School District properties. We are still doing research to learn the specifics of this past policy.

[6]According to Madison’s 2004 IPM Policy: All departments will maintain appropriate records on pest monitoring data collected, pest control actions attempted (both non-chemical and chemical), and results of pest control activity. All departments will submit by February 1st an annual report to the Public Health Commission. This report will contain the following information:

a. Completed Pesticide Application Summary for all pesticide applications made in the previous year. Application data must include: purpose, location, and amount of each pesticide product applied, including the amount of active ingredient.

b. Annual summary of non-chemical pest control activities.

c. Estimated size of the total area managed for each pest problem in a given year. The area managed will likely exceed the area treated.

d. A summary of any complaints received regarding use or the perceived need for use of pesticides, including the date complaint(s) was (were) received and thenature of the complaint(s).

e. A pest management plan for the coming year. The plan will contain the following information for each type of pest problem:

1. Definition of Roles. Identify who will: serve as the IPM Coordinator, perform pest monitoring, evaluate pest control alternatives, decide which pest control alternative to use, and implement pest control measures.

2. Pest Management Objectives. Identify the action thresholds (i.e., pest population levels) to be used to decide when some type of action should be taken to control the pest problem.

3. Monitoring Plan. Describe the methods to be used to monitor the pests and the frequency of monitoring.

4. Control Method Selection. Describe the types of pest control methods to be evaluated and the criteria used to choose the appropriate control method.

 

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