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DuPont Refuses Treatment of Toxic TCE Plume; Form Phosgene Smog Over Lake
by DuPont Profits Trump Life
Friday Jul 25th, 2014 7:55 AM
For several decades a DuPont ammunition plant in Pompton Lakes, NJ has leaked pollution into the groundwater and chemical gases (TCE, PCE and others) have seeped into resident’s basements causing cancer and other health disorders. The DuPont Corporation refuses to clean their pollution site and the EPA ignores the residents and works their magic on them with deceptive words. Latest plan for remediation by DuPont is to have the plume washed into the lake with fast moving solvents. They forgot to mention that when TCE and PCE enter the atmosphere through evaporation and sunlight exposure the result is phosgene in photochemical smog.
Background on DuPont Delays in Cleanup;

DUPONT POMPTON LAKE POLLUTION MAY BE HEADED DOWNSTREAM
DEP Scientists’ Questions Could Prompt Feds to Expand DuPont Cleanup Scope .
Posted on Jan 26, 2012
“Trenton — New Jersey state scientists have pointed to evidence that mercury from a toxic waste site at Pompton Lakes is migrating down the Ramapo and Wanaque Rivers through contaminated sediment, fish and wildlife, according to agency documents released today by Public Employees for Environmental Responsibility (PEER). These documents surface just as federal agencies are reviewing the DuPont dredging plans to determine their ecological adequacy.
Pollution from the old E.I. DuPont De Nemours & Company ammunition plant has proven to be more than a 20-year long nightmare for the 450 homes exposed to deadly vapors and other effects. Now it appears that this pollution nightmare may be spreading.
State Department of Environmental Protection (DEP) scientists found much higher levels of mercury in Pompton Lake fish than found elsewhere, raising red flags about bio-availability of the mercury and downriver sediment pollution. They said the ecological assessment in the DuPont plan to dredge a 26-acre section of Acid Brook Delta, a small part of the 260-acre polluted Pompton Lake, was “misleading” particularly in characterizing data on mercury in fish tissue. Moreover, DEP calculated a sediment cleanup standard needed to protect fish and wildlife but DuPont’s plan did not incorporate that standard.
The adjoining Ramapo and Wanaque watersheds are affected by contaminated sediment flow as are their fish and wildlife, which bio-accumulate mercury through the food chain. The current DuPont dredging plan only addresses a small portion (10%) of the Lake and does not consider downriver sediment impacts.
The U.S. Environmental Protection Agency and the U.S. Fish & Wildlife Service are now considering and must both sign off on this plan. PEER is urging Fish & Wildlife scientists to revisit the DEP standard during their review of the DuPont plan.
“These federal oversight agencies must look at these DEP findings and should conduct a de novo review of the scientific basis for the DuPont cleanup plan,” stated New Jersey PEER Director Bill Wolfe, noting that DEP had denied him access to these internal scientific documents under the state Open Public Records Act, claiming they were “deliberative” but had previously released these same documents to a different requester. “Right now we are a critical juncture in the future of Pompton Lakes.”
The DuPont plan is supposed to be based upon a site-specific ecological standard designed to protect fish and wildlife from the bio-accumulative effects of mercury in sediments. Federal review could expand the scope of the proposed cleanup and could also find additional injuries to natural resources for which DuPont must compensate the public.

For more than a century, DuPont’s operations poured heavy metals and other toxins into Pompton Lake. The plume of pollution has spread to groundwater underlying homes and businesses, causing vapor intrusion problems.”
http://www.peer.org/news/news-releases/2012/01/26/dupont-pompton-lake-pollution-may-be-headed-downstream-/

“A growing public health emergency at New Jersey’s Pompton Lakes requires the U.S. Environmental Protection Agency to step in far more aggressively than it has, according to a letter sent today by Public Employees for Environmental Responsibility (PEER). In 2010, EPA promised to provide more oversight for a long-stalled state-run clean-up of a profoundly polluted old E.I. DuPont De Nemours & Company ammunition plant but authorities still do not have a handle on worsening problems.
Hazardous materials are migrating off the 600-acre DuPont site. Volatile organic compounds from uncontrolled contaminated groundwater are migrating into at least 450 homes, exposing residents to imminent and substantial health hazards. Yet, almost three years after the vapor intrusion peril was supposedly first discovered, less than half of the homes have adequate vapor mitigation systems installed.
In a letter to EPA Regional Administrator Judith Enck, PEER urges the federal agency to invoke powers it has under national toxic clean-up laws to fully map pollution threats and to undertake speedy public health protections leading to a full clean-up. The PEER letter characterizes the 2010 EPA pledge to increase its involvement as welcome but “not nearly sufficient.”
“After more than 20 years, Pompton Lakes deserves more than additional half-way measures,” stated New Jersey PEER Director Bill Wolfe, a former analyst with the state Department of Environmental Protection (DEP), pointing out that the affected community has been cut out of official decision-making. “EPA has residual powers that it is not using – as if EPA is keeping both an arm and a leg tied behind its back.”
http://www.peer.org/news/news-releases/2011/04/11/strong-federal-action-needed-now-at-toxic-jersey-dupont-site---/

Local residents unaware of health risks, Dupont cover-up;
“DuPont Danger Was Hidden Away
In 1987, when John Sinsimer became mayor of Pompton Lakes, N.J., he had no idea about the contamination at a DuPont explosives plant and the fact that groundwater laced with toxic solvents was spreading under a nearby neighborhood. Hardly anyone was aware of it, although documents show DuPont and state environmental officials had been discussing it for several years. Three months into his term, Sinsimer learned about the contamination -- by accident -- when he found documents about DuPont locked in a Borough Hall file cabinet.”

“The topic of testing the Lakeside Middle School and its field for safety seems to be of low priority, which is again a very clear indicator that either the council does not have the willingness or fortitude to confront DuPont's toxic legacy and continue to apply pressure to ensure this polluter cleans up every inch of this town at DuPont’s expense. In my 30-plus years in this town, I played youth sports on the Barbara Drive field and every other field in the Pompton Lakes/Riverdale area. My health has declined rapidly with illness associated with living in a toxic environment.”
Patrick J. Giles,
Pompton Lakes
See more at: http://www.northjersey.com/news/217334481_Councilman_s_comments_on_DuPont_contamination_anger_reader.html


“DuPont pilot study underway in Pompton Lakes
A second pilot study to determine the best method to remove chlorinated solvents from the groundwater in the borough's Plume area is underway.
DuPont Project Manager Dave Epps (center) talks with Pompton Lakes Mayor Katie Cole about how the bioremediation process works. They are joined by George Nemethsr, an environmental scientist for O'Brien and Gere, on June 25.
In 2011, DuPont unsuccessfully performed its first pilot study that was designed to remove the Tetrachloroethene (PCE) and Trichloroethene (TCE), two chemicals that infiltrated the groundwater when the company operated a munitions factory in the borough from 1902 to 1994.
In the 1980s, the community learned that DuPont had contaminated the soil, groundwater, and the neighboring streams with these solvents, as well as lead, mercury, and other contaminants used in their manufacturing processes.

In the first pilot study, the company poured vegetable oil mixed with microorganisms into the groundwater in an attempt to remove the chlorinated solvents.
This is a process known as bioremediation, which uses microorganisms to reduce the chemical concentrations in the environment.
DuPont officials explained that his process uses microorganisms to break down the TCE and PCE into ethane, and the vegetable oil is the fuel the microorganisms need to live off of in order to continue to do this.
DuPont reported that this mixture was unsuccessful in the first pilot test because it would not move through the soil and come in contact with the TCE and PCE.
In this second pilot study, the company is mixing lactate with the microorganisms for a texture that is less viscous than the oil.
DuPont began this second pilot study on June 25 at the intersection of Barbara Drive and Schuyler Avenue. Officials said this area was chosen because it has the highest levels of TCE and PCE.
On that day DuPont Project Manager Dave Epps said the company will study this process for the next six months to determine its effectiveness.”
http://www.northjersey.com/news/215471651_DuPont_pilot_study_underway_in_Pompton_Lakes.html

http://www.northjersey.com/news/dupont-pilot-study-underway-in-pompton-lakes-1.609929?page=all#sthash.Hp6DdVOe.dpuf

“Pompton Lakes resident writes protest song about the Plume
Pete Seeger opens the show...
THURSDAY, JULY 25, 2013
BY LESLIE SCOTT
STAFF WRITER
“His name is Kenn Moutenot. He is a musician, entertainer and producer who grew up in Pompton Lakes and now lives in Bergenfield.
Over the years he has played with Dramarama, Deodato, and Buddy Miles, and is currently touring with Rick Derringer.
He will debut this song at a free gathering from 4 to 9 p.m. on Aug. 8 at Saint John's Church, 81 Christopher St., in New York City, where other artists will also perform that evening.
Moutenot explained that he was inspired to write this song after concluding that the New York-based law firm Weitz & Luxenberg, which is representing the residents of the Plume, did not have the residents' best interests at heart.
"The song is a tribute to the families of Pompton Lakes and my family of Pompton Lakes. That was the inspiration, to write the song out of frustration for unfair compensation," he said.
He said he was offered either a $1,600 settlement or medical monitoring, without holding DuPont at fault.
Moutenot said he would not agree to these terms and the law firm told him that if he did not, it would sign off on the settlement in his behalf.
"DuPont is sending these Weitz & Luxenberg lawyers to my home to try and take the lowest possible settlement, and that's their job, and I told them that right to their face, and they did not deny it, by the way," he said.
He explained that he understands that Weitz & Luxenberg is representing residents of the Plume in this lawsuit, but ultimately the law firm will be paid if and when a settlement is reached with DuPont.
He said the attorneys were pushing him to sign, and he didn't like that. So instead of getting mad, he said, he wrote a song.
"This is a song about making sure that our planet is OK for our children's children in 100 years. That is what the point is. Hey, maybe this will help bring attention and create better regulations in the future. Not that I have that much power with a song, but who knows?"

http://www.northjersey.com/news/216869421_Pompton_Lakes_resident_writes_protest_song_about_the_Plume_song_about_DuPont_lawsuit.html?c=y&page=3

http://fightforourhealth.blogspot.com/

The representative from the EPA who sounded like his name was Harry Potter (aka Uncle Harry) was working his magic on the crowd. DuPont’s solution to TCE and PCE gases in the soil vapor entering homes and making people sick was to flush it through the groundwater with a faster moving solvent. The plume with the above chemicals would then be flushed into Pompton Lakes via groundwater. At some time the volatile gas molecules of TCE and PCE would find their way to the lake’s surface and become part of the air above the lake. How long they remain there above the lake depends upon wind conditions. If it is not a windy day, a layer of photochemical smog will form and contain these products.
The health risks of inhalation of TCE and PCE include cancer and severe organ damage. Most inhalation of TCE and PCE in Pompton Lakes occurs from soil vapor entering basements and buildings. Other questions raised at the meeting left unanswered were if residents who had children that went to schools built above the plume were also at risk for cancer and deserved compensation along with the homes above the plume. If the school has a foundation with a partial basement then some TCE and PCE most likely entered the building and accumulated in the hallways. This exposes a greater amount of residents to toxins by being in public school buildings located above the plume throughout the day.
The trade-off “lesser-evilism” of not having the TCE and PCE entering basements is that of having these chemicals enter the lake and form smog above the lake’s surface. There is no question that on days with no wind there will be accumulations of TCE and PCE in the atmosphere around the lake’s surface. Since the town is near lake level and surrounds it, we can reason that some exposure to TCE and PCE will continue to occur. The best option is complete soil removal at the DuPont site paid for by the corporation, though the CEOs and top shareholders refuse to provide the needed funding to have the soil removed and taken to a proper treatment facility. The DuPont CEO is choosing to save money for the corporation at the expense of human health. To DuPont the ecosystem and human community of Pompton Lakes is disposable, their shareholder profits trumps life.

Online sources for Tetrachloroethane (TCE) and Perchloroethylene (PCE) and human health risks;

TCE in drinking water;
“Poor handling as well as improper disposal of TCE in landfills has been the main causes of groundwater contamination. The biodegradation of another volatile organic pollutant, tetrachloroethene (or perchloroethylene, PCE), in groundwater may also lead to the formation of TCE (Major et al., 1991).
1 Conversion factor in air: 1 ppm = 5.41 mg/m3 at 20 °C and 101.3 kPa (Verschueren, 1983).
In the USA, TCE has been the volatile organic contaminant that is most frequently found in groundwater and the one present in the highest concentrations (ATSDR, 1997). TCE was detected (detection limit 0.2 μg/litre) in 91 of 945 (9.6%) samples of finished water using groundwater sources nationwide. The median level in positive samples was 1 μg/litre, and the maximum was 130 μg/litre. In samples taken from tap water in homes near the Love Canal waste site, TCE levels ranged from 10 to 250 ng/litre. In New Jersey, TCE was detected in 388 of 669 (58%) samples taken between 1977 and 1979, with a maximum concentration of 635 μg/litre (ATSDR, 1997). TCE levels ranging from 900 to 27 300 μg/litre were found in contaminated wells in a survey of four states (Pennsylvania, New York, Massachusetts and New Jersey) (ATSDR, 1997). TCE was detected in 28% of 9295 surface water samples taken nationwide between 1980 and 1982 in the USA.
Due to TCE’s volatility and lipid solubility, exposure can also occur dermally and through inhalation, especially through bathing and showering. TCE is readily absorbed following both oral and inhalation exposures. Dermal absorption is also possible, but information pertaining to this route of exposure is limited.
Overall, absorption of TCE through the gastrointestinal tract is considerable and, at very low concentration, nearly complete. Once absorbed, TCE diffuses readily across biological membranes and is widely distributed to tissues and organs via the circulatory system. Primary sites of distribution include the lungs, liver, kidneys and central nervous system. TCE may accumulate in adipose tissue because of its lipid solubility. Consequently, slow release of TCE from adipose stores might act as an internal source of exposure, ultimately resulting in longer mean residence times and bioavailability of TCE (Fernandez et al., 1977; Dallas et al., 1991; Fisher et al., 1991). Age-dependent factors may influence TCE distribution in humans, suggesting greater susceptibility to TCE in children than in adults (Pastino et al., 2000).
Central nervous system effects were the primary effects noted from acute inhalation exposure to TCE in humans, with symptoms including sleepiness, fatigue, headache, confusion and feelings of euphoria (ATSDR, 1997). Simultaneous exposure to TCE and ethanol results in a marked inhibition of the metabolism of TCE, which leads to an accumulation of TCE in blood and increases the extent of central nervous system depression (Muller et al., 1975). Effects on the liver, kidneys, gastrointestinal system and skin have also been noted (ATSDR, 1997).
The authors of a retrospective cohort study conducted on 169 workers in a cardboard factory in Germany who were exposed to TCE for at least 1 year between 1956 and 1975 claim a causal link between cancer and TCE exposure (Henschler et al., 1995a,b). By the close of the study in 1992, 50 members of the study group had died, 16 from malignant neoplasms. In 2/16 cases, kidney cancer was the cause of death (SMR = 3.28, versus local population). Five workers were diagnosed with kidney cancer: four with renal cell cancer and one with a urothelial cancer of the renal pelvis (standardized incidence ratio [SIR] = 7.77, 95% CI = 2.50–18.59). After the close of the observation period, two additional kidney tumours (one renal and one urothelial) were diagnosed in the study group. By the end of the study, 52 members of the control group, which consisted of 190 unexposed workers from the same plant, had died — 16 from malignant neoplasms, but none from kidney cancer. No case of kidney cancer was diagnosed in the control group. For the seven cases of kidney cancer, the average exposure duration was 15.2 years (range 3–19.4 years).”
http://www.who.int/water_sanitation_health/dwq/chemicals/trichloroethenemay05.pdf


“PCE and TCE can also be oxidized, with second-order rate constants for reactivity with hydroxyl radicals for PCE and TCE are 2.8 x 10^9 and 4.0 x 10^9 M^-1 sec^-1. These values suggest rapid photooxidation for atmospheric PCE during daylight hours when hydroxyl radicals are formed. An estimated half-life for PCE in the atmosphere is 96 days and the degradation products are phosgene and chloroacetylchlorides. These result in the formation of photochemical smog. Though the major loss of PCE is volatization, photooxidation of PCE also occurs in surface waters exposed to sunlight, forming trichloroacetic acid.”
http://www.webpages.uidaho.edu/etox/resources/case_studies/pce_dry.pdf

http://frobbi.org/watershed/media/PoJo_02_20_05.htm

This same chemical causes problems elsewhere, looks like EPA’ Uncle Harry Potter has lost the formula for the magic potion. The EPA frequently distorts data and obfuscates reality by stretching exposure limits to favor the polluter and place the public’s health at risk. The pattern of the EPA failing to perform their job and instead pulling rabbits out of hats to benefit polluters seems to occur nationwide.

EPA lowers standards to benefit polluters in NY;
“People living at polluted sites nationwide could be exposed to the toxin trichloroethylene, or TCE, at levels higher than the Environmental Protection Agency identified as a health concern in 2001, because the EPA never set new cleanup standards based on its study.
The health-risk analysis that identified the danger TCE posed to those who breathe even minute amounts was never translated into EPA policy, despite the recommendation of its own Science Advisory Board. At the prompting of industry and other federal agencies, the EPA has subjected the analysis to a review by the National Academy of Sciences.
That review will take more than a year, leaving those who live at polluted sites and the agencies responsible for remedying them using cleanup guidelines for the ubiquitous solvent that vary from state to state, and even within the boundaries of one town -- East Fishkill in Dutchess County.
In East Fishkill, the EPA has committed to removing all TCE vapors it can detect in the Hopewell Precision neighborhood, where groundwater is polluted with TCE.
EPA spokesman James Haklar described this as a "pro-active" approach, determined by aspects specific to that site, that will address homes where there is a "potential impact." It also ultimately saves money because it will reduce long-term monitoring costs.
In the same town, a few miles to the south, the EPA could permit TCE vapors to remain in homes in the Shenandoah neighborhood, as long as they don't exceed New York's guideline of 5 micrograms per cubic liter -- about 13 times higher than the smallest detectable concentration.
Vapors of TCE and/or a related chemical have been detected beneath 14 homes there, and the EPA plans to test inside homes before the end of winter.
The apparent discrepancy is based on conditions specific to the two sites, including that TCE is the main contaminant at the Hopewell Precision site, but a secondary contaminant in the Shenandoah neighborhood, Haklar said.
Some residents, however, are outraged the EPA won't commit to cleaning their air as much as the agency will in their neighbors' homes.
"It's not a case that the danger is not there. It's more a case of whom are we protecting," said Denis Callinan, who lives in Shenandoah. "It's obvious we are protecting the federal government because they are one of the worst polluters ... and we are definitely protecting major industry."
The discrepancies only grow with the miles.
In Endicott, about 180 miles away, New York and IBM Corp. are using the state's guidelines -- though residents there have been outraged since learning of the EPA's goal at the Hopewell Precision site in East Fishkill. Groundwater there is polluted with TCE from an old IBM facility and vapors have seeped into hundreds of homes.
"It is ludicrous to me that there are different standards," said Betty Hicks, whose home in Hopewell Precision is being ventilated to reduce vapors. "People in Appalachia should die, and people in Scarsdale shouldn't die? It's ridiculous."
State and federal elected officials have called for clearer, national standards.
National standards lacking
With the EPA's health-risk analysis in limbo, there are no national standards that dictate when the EPA should take action to clean a site, nor are there national guidelines for how thoroughly sites should be cleaned.
The EPA uses a variety of guidelines, which can vary among the agency's nine regional offices, to determine which sites need to be cleaned, and to what extent.
- TCE is far more toxic than thought -- "highly likely" to cause cancer and linked to a variety of toxic effects on the nervous, immune, reproductive and other body systems.
- Breathing TCE was identified as a potent risk, even at very small concentrations.
The EPA normally sets cleanup standards for polluted sites based on risk analyses. The EPA sets its standards to reduce exposure to the point where no more than one in 10,000 adults would be expected to get cancer if a 150-pound adult was exposed for a lifetime -- 24 hours a day for 30 years.
In this case, TCE cleanup standards for contaminated air would have been so low, the most sensitive instruments could not always detect harmful concentrations.
- Some of TCE's toxic effects are likely to be greater on children and adults with certain diseases, including diabetes.
- Effects are likely to be exacerbated by exposure to other chemicals, including alcohol and other chlorinated solvents.
When the body metabolizes any of the three chemicals -- TCE, PCE or TCA -- the same substance, trichloroacetic acid, is formed, though at different rates for each chemical. Trichloroacetic acid can also form as a byproduct of chlorinating drinking water.
Trichloroacetic acid is the metabolite associated with TCE that is most analyzed for its potential to cause cancer. The EPA's 2001 draft analysis of TCE health risks identified the cumulative exposure to different chemicals as a concern, in part, because of the way they interact when the body metabolizes them.
Critics: Cost is issue
That hasn't stopped critics from charging the departments of Defense and Energy are less concerned about sound science than saving money. The federal government is responsible for at least 46 Superfund sites with TCE, many of them at Air Force bases, according to an EPA database. More strict cleanup standards would drive up costs.
This isn't the first EPA risk analysis to get caught in limbo amid controversy, Sass said. The EPA's cancer risk guidelines have yet to be updated. Based on the agency's 1999 proposed guidelines, TCE would be considered "highly likely" to cause cancer. Under the "current" 1986 guidelines, TCE is considered a "probable human carcinogen."
http://frobbi.org/watershed/media/PoJo_02_20_05.htm

During the meeting Harry Potter claimed that TCE and PCE do not bioaccumulate in fish and simply evaporate into the air. He forgot to mention the additional reaction and formation of phosgene as a degradation product from UV oxidation of PCE in sunlight with hydroxyl radicals (OH)-.

UV oxidation and phosgene health effects;
“The UV oxidation causes organic pollutants to enter excited states, and subsequently undergo series of free-radical chain reactions, whereby they are decomposed. The general understanding is that under UV oxidation a molecule undergoes metastasis into the excited state after absorbing photons, per the Gottus–Draper and Einstein–Stark theories.”
http://wenku.baidu.com/view/846578a3284ac850ad0242a1


“Most PCE is introduced into the atmosphere by evaporative losses. PCE degradation into the atmosphere, which has an estimated half-life of 96 days in typical ambient air, is the result of reaction with hydroxyl radicals. Phosgene and chloroacetylchlorides are degradation products of this reaction.”
http://www.tftptf.com/images/ABC_PHA_1990.pdf


Health effects of phosgene exposure;

“Phosgene is a highly toxic substance that exists as a gas at room temperature. Owing to its poor water solubility, one of the hallmarks of phosgene toxicity is an unpredictable asymptomatic latent phase before the development of noncardiogenic pulmonary edema.

Signs and symptoms

According to the National Institute for Occupations Safety and Health (NIOSH), a toxic level that can place a person’s life and well-being in jeopardy can be as low as 2 parts per million (ppm).[1] Exposure to moderate-to-high concentrations of phosgene (>3-4 ppm) can produce an immediate irritant reaction that typically lasts 3-30 minutes and includes the following:

•Lacrimation
•Conjunctival irritation/burning
•Burning sensation in mouth/throat
•Throat swelling/changes in phonation - May reflect laryngeal edema

Respiratory manifestations, which can develop relatively early at greater than 4.8 ppm,[2] usually do not develop until after a latent period lasting 4-24 hours postexposure. They consist of the following signs and symptoms:

•Cough - Initially dry, then increasing frothy white/yellow sputum
•Chest tightness, chest pain, or substernal burning
•Dyspnea - Exertional early on, subsequently becomes present at rest
•Altered taste sensation - If the patient is a smoker, metallic or unpleasant taste to cigarettes

Other signs and symptoms of this phase, which result primarily from hypoxemia or volume depletion, include the following:

•Lightheadedness
•Palpitations
•Angina
•Headache
•Anorexia
•Nausea, and vomiting
•Weakness
•Anxiety and sense of impending doom
On physical examination, respiratory findings may include the following:

•Crackles on auscultation - Herald the onset of pulmonary edema
•Cyanosis - Late finding
•Thin, frothy white/yellow secretions
•Wheezing
•Tachypnea
•Stridor
•Accessory muscle use for respiratory effort

Cardiovascular findings may include the following:

•Tachycardia
•Hypotension - Late finding secondary to inflammation-mediated fluid diversion out of vascular system and into lung interstitium

Skin findings may include the following:

•Cyanosis from pulmonary injury and resultant hypoxemia

Three patients in China were exposed to an unknown concentration of phosgene gas in an industrial accident. Their immediate symptom was eye irritation, and they were properly decontaminated. However, the symptoms of cough, chest tightness, and dyspnea did not occur until 8-12 hours later.[2]

In another recent incident, a young Indian worker was exposed to phosgene gas at a pesticide manufacturing factory. Initial symptoms consisted of lacrimation, nausea, and a burning sensation in the mouth and throat with a dry cough. Six hours post exposure he began experiencing breathlessness. Twenty-four hours after exposure, he developed acute respiratory distress (pulse, 130/minute; respiratory rate, 36/minute; blood oxygen saturation [SpO2], 80% on room air), which ultimately required invasive airway management.[3]

http://emedicine.medscape.com/article/832454-overview



Here is the shorthand equation for (PCE) perchloroethylene PCE (C2Cl4) plus reactive hydroxyl (OH-) and oxygen (O2) forming phosgene gas (COCl2) and hydrochloride (HCl 2) and carbon dioxide (CO2). The error statement indicates it should be written as two different reactions, though this is a simplified version;


C2Cl4 + OH{-} + O2 = COCl2 + HCl 2 + CO2

Error: equation C2Cl4+OH{-}+O2=COCl2+HCl 2+CO2 can be balanced in an infinite number of ways: this is a combination of two different reactions.

http://www.webqc.org/balance.php


Online sources for PCE forming phosgene gas;

“The fate of atmospheric phosgene and the stratospheric chlorine loadings of its parent compounds: CCl4 , C2 Cl4 , C2 HCl3 , CH3 CCl3 , and CHCl3

A study of the tropospheric and stratospheric cycles of phosgene is carried out to determine its fate and ultimate role in controlling the ozone depletion potentials of its parent compounds (CCl4, C2Cl4, CH3CCl3, CHCl3, and C2HCl3). Tropospheric phosgene is produced from the OH-initiated oxidation of C2Cl4, CH3CCl3, CHCl3, and C2HCl3. Simulations using a two-dimensional model indicate that these processes produce about 90 pptv/yr of tropospheric phosgene with an average concentration of about 18 pptv, in reasonable agreement with observations. Our results are potentially sensitive to a variety of parameters, most notably the rate of reaction of phosgene with sulfate aerosols. However, on the basis of the observed vertical distribution of COCl2, we estimate that the reaction of COCl2 with sulfate aerosol most likely has a γ<5×10-5 and, as a result, has a negligible impact on the stratospheric chlorine loadings of the phosgene parent compounds. -from Authors

Duke Authors
## Chameides, William

Cited Authors
## Kindler, TP; Chameides, WL; Wine, PH; Cunnold, DM; Alyea, FN; Franklin, JA

Published Date
## 1995

Published In
## Journal of Geophysical Research

Volume / Issue
##100 / D1

Start / End Page
##1235 - 1251

Citation Source
##SciVal

https://scholars.duke.edu/display/pub764482

http://onlinelibrary.wiley.com/doi/10.1029/94JD02518/abstract;jsessionid=80CEB873D23EFC6D3AAD00DF6FEF8C0F.f04t04?deniedAccessCustomisedMessage=&userIsAuthenticated=false




http://www.atmos-chem-phys.net/11/2371/2011/acp-11-2371-2011.pdf

http://books.google.com/books?id=fM43Ny2eFS8C&pg=PA162&lpg=PA162&dq=C2Cl4+%2B+OH-+%3D+tropospheric+phosgene&source=bl&ots=-nw7PfOYeD&sig=lfbKwg0LDju3PErImR1HD3bT4bk&hl=en&sa=X&ei=mUTSU5-aBejisAT_oIHgCw&ved=0CD0Q6AEwAw#v=onepage&q=C2Cl4%20%20%20OH-%20%3D%20tropospheric%20phosgene&f=false

Phosgene: And Related Carbonyl Halides
By T.A. Ryan, E.A. Seddon, K.R. Seddon, C. Ryan



Q: How long before PCE converts to phosgene in the air?
A: 2-3 months.

ATMOSPHERIC PERSISTENCE

The dominant tropospheric loss process for tetrachloroethylene is expected to be by reaction with the hydroxyl (OH) radical. The calculated half-life and lifetime for tetrachloroethylene due to gas-phase reaction with the OH radical are 2 months and 3 months, respectively (Atkinson, 1995). Both nitrate radical and ozone chemical reaction removal processes are too long to compete with the OH radical reaction. Tuazon et al. (1988) showed that the reaction of the OH radical with tetrachloroethylene generated chlorine atoms and that in the atmosphere the reaction forms phosgene and hydrogen chloride as well as other, as yet unidentified, products. Therefore, tetrachloroethylene is sufficiently persistent to be transported throughout an air basin before it is degraded (ARB, 1991b).

Cancer: Epidemiological studies have provided some indication that the use of dry cleaning solvents, primarily tetrachloroethylene, poses an increased risk of cancer for exposed workers. (U.S. EPA, 1994a).


http://scorecard.goodguide.com/chemical-profiles/html/tetrachloroethylene.html

http://www.macehead.org/index.php?option=com_docman&task=doc_view&gid=450&Itemid=73


The use of phosgene gas was in WW1 by Germans and French due to trench warfare stalemates. Soldiers exposed to phosgene in small undetectable amounts (0.4) parts per million (ppm) were already getting above safe doses. Phosgene was also inhaled with a delayed reaction time as much as 48 hours, causing damage to lungs before being noticed. Those soldiers exposed without detecting phosgene died from having water in their lungs.

Phosgene in WW1;

“Phosgene was the next major agent employed, again used first at Ypres by the Germans in December 1915 (although some sources state the French were the first to employ it). Phosgene is a colourless gas, with an odour likened to that of ‘musty hay’. For this odour to be detectable, the concentration of phosgene actually had to be at 0.4 parts per million, several times the concentration at which harmful health effects could be expected. It is highly toxic, due to its ability to react with proteins in the alveoli of the lungs and disrupt the blood-air barrier, leading to suffocation.

Phosgene was much more effective and deadly than chlorine, though one drawback was that the symptoms could sometimes take up to 48 hours to manifest. Its immediate effects are coughing, and irritation to the eyes and respiratory tract. Subsequently, it can cause the build-up of fluid in the lungs, leading to death. It’s estimated that as many as 85% of the 91,000 deaths attributed to gas in World War 1 were a result of phosgene. It’s hard to put a precise number on, since it was commonly used in combination with chlorine gas, along with the related chemical diphosgene. Combinations of gases became more common as the war went on. For example, chloropicrin was often used for its irritant effects, and its ability to bypass gas masks, causing sneezing fits which made soldiers remove their masks, exposing them to poison gases.”

http://www.compoundchem.com/2014/05/17/chemical-warfare-ww1/


“Phosgene was especially potent as its impact was frequently felt only 48 hours after it had been inhaled and by then it had already bedded itself in the respiratory organs of the body and little could be done to eradicate it. Also it was much less apparent that someone had inhaled phosgene as it did not cause as much violent coughing. By the time that phosgene had got into a person's bodily system, it was too late.”

http://www.historylearningsite.co.uk/poison_gas_and_world_war_one.htm



Though the amount of phosgene formed by DuPont’s pollution plume’s chemical reaction above Pompton Lakes will not compare to the amounts used in WW1’s trench warfare, it remains the same substance. How unfortunate that the DuPont Corporation’s ammunition plant used during WW2 against the Nazis is now inadvertently creating the same chemical weapon used in WW1 by Germany. The only reason for this accidental formation of phosgene smog in Pompton Lakes is their unwillingness to pay for proper disposal of the soil plume contaminated with TCE and PCE. If DuPont claims the lesser evil approach of flushing the TCE and PCE away from the homes, they argue in favor of low grade long term chemical warfare above the surface of Pompton Lake.

The residents and ecosystems of Pompton Lakes, NJ need help to urge DuPont to do the right thing and clean up their mess by soil removal and decontamination.
Please tell DuPont to remove the contaminated soil plume from Pompton Lakes!

Local activists CCPL;
http://www.theccpl.org/