Welch Group Environmental and its owner, Glenn Welch, are accused in a federal indictment of violating the Clean Air Act and storing and disposing of hazardous waste without a permit.

Belton, SC businessman accused of mishandling lead from shooting ranges

Welch Group Environmental occupied this building on Belton Highway before going out of business. The company and its owner, Belton resident Glenn Welch, are accused in a federal indictment of violating the Clean Air Act and storing and disposing of hazardous waste without a permit.

Posted: July 16, 2016
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By Kirk Brown of the Independent Mail

Truckloads of bullets collected from shooting ranges were shoveled into the caldron nestled in a wooded area near Fair Play.

A kerosene jet heater was used to melt the bullets. Then workers with Welch Group Environmental would use one-gallon paint cans to scoop molten lead into molds, creating 25-pound ingots that the company sold.

At one point, the company was melting down 10,000-15,000 pounds of lead each week. And its workers were being exposed to dangerous fumes at levels exceeding federal standards, according to a 2011 report from the U.S. Department of Labor's Occupational Safety and Health Administration.

Now the company's owner, Belton resident Glenn Welch, is facing up to up to $800,000 fines and as many as 20 years in prison in connection with a federal indictment issued last week.

The indictment accuses Welch and his company of violating the Clean Air Act at two locations in Anderson County between November 2010 and May 2011. The indictment also says that Welch and his company knowingly placed another person in imminent danger of serious bodily injury.

Further, the indictment alleges, Welch and his company stored and disposed of hazardous waste without required permits.

Welch refused to answer any questions when approached by a reporter at his home, which sits on a two-acre tract along White Oak Road. The property has a market value of $407,000, according to county land records.

Last week's indictment comes after OSHA levied $500,000 in fines against Welch's company. The fines stem from 33 health violations discovered during inspections in 2010 and 2011 at its facilities in Anderson County and at a shooting range in Florida that the company was hired to clean.

Most of the health violations involved Welch Group Environmental employees being overexposed to lead. The company also was cited for failing to ensure that its workers were wearing properly fitted face-mounted respirators.

Prolonged exposure to lead can cause serious health issues in adults, including problems with concentration, high blood pressure, heart and kidney disease and reduced fertility, according the U.S. Centers for Disease Control and Prevention in Atlanta.

Eight of the company's employees who were cleaning the Delray Shooting Center in Delray Beach, Florida, had elevated lead levels in their blood, according to OSHA. At least two employees were exposed to more than nine times the permissible limit for lead while shoveling and sweeping at the shooting range.

Welch, who used to run a restaurant across the street from Belton City Hall, created Welch Group Environmental in 2006 to remove lead from shooting ranges across the nation.

An estimated 20 million gun enthusiasts visit 9,000 shooting ranges in the U.S. annually, and they generate thousands of tons of lead waste, according to the National Shooting Sports Foundation and the federal Environmental Protection Agency. Lead contamination has become a growing concern at some older shooting ranges, including a pair near San Francisco where cleanup costs have topped $20 million at each site.

Welch's company was housed in a building on Palmetto Parkway in Belton when a worker was burned in a June 2008 "flash fire," said Alan Sims, the city's fire chief.

Welch Group Environmental later moved to another building at 5034 Belton Highway near Neals Creek Baptist Church.

After being cited for health violations by OSHA, Welch Group Environmental was sued in Anderson County for failing to fully pay its worker compensation insurance premiums. Commerce and Industry Insurance Co. won a $29,927 judgment against the company in August 2012, court records show.

That same year, EPA officials sought help from the U.S. Coast Guard's Gulf Strike Team to help clean up the Welch Group Environmental site near Fair Play. The unit specializes in responding to environmental incidents.

Welch was among the featured speakers at Lead Management & OSHA Compliance workshops hosted by the National Shooting Sports Foundation in St. Louis and Atlanta in 2013 and in Charlotte last year, according to new releases from the organization. A spokesman for the foundation, which serves as the trade association for the firearms industry, did not respond to a phone message or email.

Welch Group Environmental went out of business before paying all of the fines levied by OSHA, agency spokesman Michael D'Aquino said in an email.

Last week, no one was in the locked building that the company previously occupied on Belton Highway. Through a broken window, rows of drums could be seen in a darkened garage.

A woman was killed and six people - including five children - were injured after a van collided with a semi truck in Interstate 80/94

Police: Woman killed, 6 injured in I-294 crash near South Holland







Sun-Times Media Wire
Updated 1 hr 18 mins ago
SOUTH HOLLAND, Ill. -- A woman was killed and six people - including five children - were injured in a crash on Interstate 80/94 in the south suburbs Monday evening, police said.

The crash occurred near Route 394 about 5:18 p.m., according to Illinois State Police. All westbound lanes remained closed as of 9 p.m.

A van carrying two adults and five children collided with a semi truck in the westbound lanes of the interstate near Route 394 about 5:20 p.m., according to Illinois State Police. The van rolled over during the crash and the woman driving the van was taken to an area hospital in serious condition, where she later died.

The Cook County medical examiner's office did not confirm death Monday night.

The other adult and five children were hospitalized with injuries not believed to be life-threatening, police said.

State police were working to recreate the crash to determine its cause. Lanes were expected to be reopened by 9:30 p.m., police said.

(Source: Sun-Times Media Wire - Copyright Chicago Sun-Times 2016.)

Driver critically injured after the truck went off the road, hit several trees and burst into flames on I-95 in Cumberland County, NC

A truck went off the road and burst into flames on I-95 in Cumberland County.

By Heather Waliga
Updated 2 mins ago
FAYETTEVILLE (WTVD) -- A truck driver was severely burned Monday evening in a tractor-trailer accident on Interstate 95.

It happened about 6:15 p.m. on I-95 South near mile marker 58 in Cumberland County.

A spokesman for the North Carolina Highway Patrol said the 2013 Freightliner ran off the road on the right shoulder and jackknifed into the woods. It then burst into flames.



Eyewitnesses told state troopers that the vehicle suddenly reduced speed and ran off the road to the right and traveled down an embankment, striking several trees before becoming engulfed in flames





A truck driver had to be life-flighted to UNC Burn Center after this fiery crash Monday.

The truck driver, identified as Gale Bernard Beasley, 61 of Clayton, was able to get out of the cab but suffered severe burns.

Beasley was life-flighted to UNC Burn Center.





Firefighters work the scene of the crash.

The southbound lanes of I-95 were closed for about 90 minutes. Traffic was directed off of I-95 south at both exits 61 and 65. All lanes of I-95 are now open and flowing, however the clean up continues on the shoulder of I-95.

4 kids, 2 adults hospitalized after drunk driver loses control of minivan on Staten Island and crashes into a utility pole

Eyewitness News
Updated 1 hr 10 mins ago

GRASMERE, Staten Island (WABC) -- A 35-year-old man lost control of a minivan while driving on Fingerboard Road on Monday afternoon, crashing into a utility pole on Staten Island.

The crash happened around 4:30 p.m. near 338 Fingerboard Road in the Grasmere section.

There were five passengers inside the minivan at the time - a 11-month-old girl, a 3-year-old girl, a 9-year-old boy, an 11-year-old girl and a 33-year-old woman. All were taken to Staten Island hospital in critical, but stable condition.


The driver is currently in police custody at Staten Island North Hospital, and is expected to be charged with DWI.

Tree worker killed after he fell from a bucket truck while he was cutting down trees in Lindenhurst, Long Island, NY

Long Island Tree Worker Dies in Fall From Bucket Truck


Police on Long Island are investigating the death of a man who fell from a bucket truck while he was cutting down trees. (Published Friday, July 15, 2016)

Police on Long Island are investigating the death of a man who fell from a bucket truck while he was cutting down trees.

Suffolk County police say 35-year-old Oscar Martinez was cutting trees in Lindenhurst just before 3 p.m. Friday when he fell from elevated bucket of the truck.

He was working for Long Island Garden and Tree Service of Brentwood, NY.

Martinez, of Brentwood, was taken to Good Samaritan Hospital Medical Center in West Islip. He was pronounced dead there.

Police say the death was apparently accidental.

The Occupational Safety and Health Administration has been notified.

NIOSH REPORT: FDNY FIRE OFFICER LINE OF DUTY DEATH

NIOSH REPORT: FDNY FIRE OFFICER LINE OF DUTY DEATH

July 16, 2016


On July 05, 2014, 40-year-old FDNY Lieutenant Gordon “Matt” Ambelas was overcome by extreme fire conditions while attempting to find the seat of the fire. Ambelas, 40, left behind a wife, Nanette, and two young daughters, Gina and Gabby, went into cardiac arrest after suffering smoke inhalation and third-degree burns on his head.

The 14-year FDNY veteran had been promoted to lieutenant just 10 months ago.

The fire was located in the bedroom of a 500-square-foot apartment on the 19th floor of a 21-story residential apartment building. The apartment was extremely cluttered with personal possessions stacked high against all walls, making travel through the apartment difficult. The Lieutenant and his Ladder 119 crew forced the door to the fire apartment and entered to search for the seat of the fire. The Engine 211 lieutenant and fire fighter followed them into the apartment with a charged hoseline.

Due to the cluttered conditions, which limited their mobility, crews had trouble locating the seat of the fire. Visibility was limited due to the thick, optically-dense smoke. The conditions inside the apartment rapidly deteriorated, forcing both crews to withdraw to the hallway. The Engine 211 lieutenant radioed a Mayday and stated he had fire behind him. 

All fire fighters in the apartment were able to withdraw except for the Ladder 119 lieutenant. Engine 211 re-entered the apartment and extinguished the fire. A fire fighter reported hearing a PASS device in the direction of the bedroom. The Ladder 119 lieutenant was found a short time later, unresponsive and with his facepiece dislodged from his face. 

He was immediately transported to a local hospital where he was pronounced dead. RIP.

REPORT: https://www.cdc.gov/niosh/fire/pdfs/face201414.pdf

 

A hit and run crash left an EMT critically injured and several other people hurt in Grand Prairie in Texas

EMT CRITICAL-STRUCK AT TEXAS CRASH SCENE

July 16, 2016


A hit and run crash left an EMT critically injured and several other people hurt in Grand Prairie (Texas) when someone in a pickup truck plowed through a crash scene. EMT Dalton Terrell sustained a traumatic brain injury, broken ribs, lacerated liver and other injuries when he was hit.

Dalton was one of the EMTs on duty working for the Yello Belly Dragstrip in Grand Prairie last Sunday night when a there was a wreck just outside the gates. Dalton and his partner went to help when another truck plowed into the scene. He still has a long recovery ahead. He had to have surgery to repair a torn artery in his brain. But his neurosurgeon said the young father’s prognosis is good.

The driver responsible for injuring all those people is on the run. Grand Prairie police say they have a good idea of who the driver is and just have to find him to make the arrest.

Dalton’s family was told the company did not have workman’s comp insurance. The family will be financially responsible for his medical and hospital stay. A GoFundMe page (link below) has been set up to help with medical bills.



VIDEO FROM THE CRASH SCENE

http://www.fox4news.com/news/175005590-story

+++Family Needs Help+++

https://www.gofundme.com/DaltonTerrell

Semi-truck knocked out several steel girders as it passed under a railroad bridge and stuck under 63rd Street rail bridge on South Side of Chicago

Updated 2 hrs 27 mins ago
CHICAGO (WLS) -- A semi truck driver knocked out several steel girders as he passed under a railroad bridge at West 63rd Street in Chicago's Englewood neighborhood, a spokesperson from Norfolk Southern Corp. said.

The spokesperson said the container being hauled was too tall to fit under the bridge, which is operated by Norfolk Southern.

Officials said 63rd will be closed to traffic between South State Street and South Wentworth Avenue until crews remove the debris and engineers assess the damage. Norfolk Southern employees were on site as of 1:30 p.m. Thursday.

The bridge has been closed to rail traffic for the last four months and is scheduled to be demolished this year, the spokesperson said. The railroad planned to have a new bridge in place by 2017.

One person was injured and Blue Line service was disrupted after a Forest Park-bound train derailed by a loose tire from a box truck

One person was injured and Blue Line service was disrupted after a Forest Park-bound train derailed Monday morning. (WLS)

By Leah Hope
Updated 6 mins ago
CHICAGO (WLS) -- One person was injured and Blue Line service was disrupted after a Forest Park-bound train derailed Monday morning just before the Illinois Medical District station.

Illinois State Police said a tire from a box truck on the Eisenhower Expressway dislodged and ended up on the CTA tracks, causing the first train car to derail.




Blue Line service was suspended for nearly three hours between UIC Halsted and Pulaski due to the derailment. Shuttle buses were put in place to help passengers travel between the impacted stations.


Officials said 61 passengers on board the train refused treatment. One passenger was taken to a local hospital with minor injuries.

State police said they are continuing to investigate. No citations have been issued.

7 children were injured, one seriously, after their SUV was T-boned by a pickup truck in Lynbrook, Long Island, NY

N.J. Burkett has the latest details.

By N.J. Burkett and Eyewitness News
Updated 53 mins ago
LYNBROOK, Long Island (WABC) -- Seven children were rushed to area hospitals, one airlifted in serious condition with head trauma after their SUV was struck broadside by a pickup truck in Lynbrook on Monday afternoon.

The crash happened at 1 p.m. at Peninsula Boulevard at Lyon Place.

The children, whose names have not been released, were all passengers in a Ford Explorer, with a male driver and a female passenger. Authorities tell Eyewitness News that one child may have been sitting on a passenger's lap.

The driver of the pickup, a Ford F-150, was alone in the vehicle and was not injured.

Chief Joseph Neve of the Lynbrook Police Department says that the SUV was traveling southbound on Peninsula when it was struck by the pickup, which was making a left turn onto Lyon Place from the northbound lanes of the boulevard.

The children range in age from nine to fourteen and their conditions could not immediately be confirmed.

The boulevard is shut down southbound at the scene.

Charges have not been filed, although the investigation is ongoing.

PADEP and Stonehenge Appalachia LLC agree to $1.5 Million Civil Penalty for Environmental Violations

COMMONWEALTH OF PENNSYLVANIA
Dept. of Environmental Protection
Commonwealth News Bureau
Room 308, Main Capitol Building
Harrisburg PA., 17120

FOR IMMEDIATE RELEASE
07/18/2016


CONTACT:

Melanie Williams, DEP

814-332-6615


DEP and Stonehenge Appalachia LLC agree to $1.5 Million Civil Penalty for Environmental Violations


HARRISBURG, PA - The Pennsylvania Department of Environmental Protection (DEP) and Stonehenge Appalachia LLC, (Stonehenge) have entered a Consent Order and Agreement that includes a $1.5 million civil penalty assessment for having uncontrolled and unpermitted sediment discharges into wetlands and causing a landslide into a stream in Butler County.

“This type of man-made ecological impact is both egregious and avoidable, and never should have occurred,” said Acting DEP Secretary Patrick McDonnell. “By this action, Stonehenge accepts both environmental and financial responsibility for their actions.”

In March 2016, DEP issued a Cease and Desist Order to Stonehenge and its contractors for violating environmental regulations at various stream and wetland crossings an along 18-mile pipeline in Butler County. The violations took place between November 2015 and March 2016. Stonehenge appealed the Orders.

The DEP determined that Stonehenge caused uncontrolled and unpermitted discharges of sediment along the 18-mile pipeline, caused a large landslide of sediment into a stream, and filled two wetlands with sediment. The company’s pipeline directional boring activities also discharged significant drilling fluids, including bentonite clay into waters of the Commonwealth. These activities violate the 2012 Oil and Gas Act, Clean Stream Law, Dam Safety and Encroachments Act, and the Solid Waste Management Act.

The Consent Order and Agreement documents the restoration and mitigation activities that have been taken by Stonehenge to address the violations and outlines additional restoration obligations. The $1.5 million civil penalty is assessed under the 2012 Oil and Gas Act, Clean Streams Law, the Dam Safety and Encroachment Act, and the Solid Waste Management Act. As part of the Consent Order and Agreement, Stonehenge will withdraw the appeal of the DEP Orders and the DEP will continue the review of the permit applications submitted by Stonehenge for pipeline projects in Butler County. Stonehenge’s Butler County pipeline projects will gather and compress natural gas from multiple wells in various townships in Butler County, and will then deliver the gas to a local processing plant.


###

THE TEFLON LEGACY: Dupont and Dow Chemical are facing exposure to costly potential damages from claims that perfluorooctanoic acid (PFOA), a chemical used to make Teflon, caused cancer and other ailments

Dupont and Dow Chemical must tell shareholders before next week’s merger vote that they may face exposure to costly potential damages from claims that a chemical used to make Teflon caused cancer and other ailments, community activists told the companies.

While DuPont is the named target of the 3,500 lawsuits filed by people living near a Teflon plant in Parkersburg, West Virginia, it has claimed Chemours, a spinoff it created last year, was required to pay any damages. Chemours said last week it might fight efforts to force payment, saying it “retains legal defences” to DuPont’s claims of indemnification.

DuPont and Dow should tell shareholders before the July 20 vote on the $59bn merger that the combined firms could end up getting stuck with the bill, Action Fund Network and Keep Your Promises DuPont wrote.

The merger partners must also share updated federal guidance on how much of the Teflon chemical people can safely be exposed to and the potential liability at 19 polluted sites, the activists wrote in a letter published in DuPont regulatory filing on Friday. The undisclosed items “are substantial, material liabilities that DuPont faces as a result of its decades-long contamination caused by perfluorooctanoic acid (PFOA), which Dow shareholders stand to inherit,” the groups said.

DuPont said in the filing that it had disclosed all the information necessary under federal law. The Wilmington, Delaware-based company remains “committed to fulfilling all our legal and environmental obligations as it relates to PFOA,” spokesman Dan Turner said.

Representatives of Dow and Chemours did not respond to requests for comment.

Potential payments related to health claims from exposure to the Teflon chemical could reach $1.9bn, according to Bloomberg Intelligence. DuPontlast week was ordered by an Ohio jury to pay more than $5.5m to a man who developed testicular cancer after drinking water polluted with PFOA. It was the sixth case to be resolved, with 40 more scheduled for next year.

It makes sense that Chemours would try to break the indemnification clause in last year’s separation agreement as the potential liability is the biggest drag on the stock price, said Christopher Perrella, an analyst at Bloomberg Intelligence. While shares rose earlier this year, they are down 57% since debuting in June 2015.

“It may be hard for Chemours to get out from under it unless they go bankrupt,” Perrella said.


Source: http://www.bdlive.co.za, July 18, 2016
By: Jack Kaskey and Tiffany Kary







====================







Perfluorooctanoic acid (PFOA, or C8) is a synthetic chemical used since the late 1940s in manufacturing industrial and household products (Steenland et al. 2010). It is persistent in the environment and has a long human half-life (Lau et al. 2007; Olsen et al. 2007; Seals et al. 2011). PFOA is found at low levels in the serum of most people living in the United States, with higher levels observed in occupationally exposed workers (Calafat et al. 2007; Lau et al. 2007). Exposure sources in the general population are not well established, but likely include diet, drinking water, food packaging, and household products (Lau et al. 2007). PFOA was reported to induce liver, testes, and pancreatic tumors in male rats over a 2-year period (Biegel et al. 2001). However, no evidence was found of hepatocellular, testicular, or pancreatic tumors in male monkeys exposed to PFOA for 26 weeks and observed for 90 days after exposure (Butenhoff et al. 2002). Exposure levels used in the animal studies were higher than human levels typically seen from drinking water or occupational exposure. Because of PFOA’s potential for environmental persistence, long human half-life, and possible toxicity, there is rising concern about whether it might be associated with human cancers (U.S. Environmental Protection Agency 2005, 2006).

The biologic mechanisms by which PFOA caused rat tumors, as well as the pertinence of the animal findings to humans, are unclear. PFOA activation of peroxisome proliferator receptors may cause liver tumors in rats (Kennedy et al. 2004), and also in rats, PFOA-induced increases in serum estradiol levels (Biegel et al. 2001) may have caused testicular tumor growth. It is not known if these processes are relevant to human cancer (DeWitt et al. 2009; Koeffler 2003; Suchanek et al. 2002).

Most previous human studies of the association between PFOA and cancer have been mortality studies of occupationally exposed workers with few cancer deaths. One study followed workers employed at a Minnesota PFOA production plant between 1947 and 1997 (Lundin et al. 2009). These investigators reported some evidence of positive trends for prostate and pancreatic cancer across job categories with increasing PFOA exposure, but estimates were based on only 16 and 13 deaths, respectively.

A second mortality study followed workers who had been employed at any time between 1948 and 2002 at the West Virginia DuPont Washington Works plant considered in the present study (Leonard et al. 2008). These authors reported that kidney cancer mortality was almost doubled among plant workers compared with other regional DuPont workers [standardized mortality ratio (SMR) = 181.0, 95% confidence interval (CI): = 93.5, 316.2]. Steenland and Woskie (2012) recently updated this study and reported a significant increase in kidney cancer mortality with increasing estimated cumulative PFOA serum concentrations based on 12 kidney cancer deaths. SMRs (95% CIs) by increasing exposure quartile were 1.07 (95% CI: 0.02, 3.62), 1.37 (95% CI: 0.28, 3.99), 0 (95% CI: 0, 1.42), and 2.66 (95% CI: 1.15, 5.24) (trend test p = 0.02).

There have been two PFOA–cancer incidence studies among general populations: Eriksen et al. (2009) and Bonefeld-Jorgensen et al. (2011). Eriksen et al. (2009) enrolled 57,053 cancer-free Danish adults 50–65 years of age; they measured PFOA plasma concentrations during enrollment and followed participants for approximately 10 years for incident prostate, pancreas, liver, and bladder cancers. Positive associations between PFOA and prostate and pancreatic cancers were reported but were not significant, and no significant linear trends were seen for any of the four cancers. A case–control study of 31 breast cancer cases from the Inuit population (Bonefeld-Jorgensen et al. 2011) reported no relationship between PFOA and breast cancer. The unadjusted odds ratio (OR) was 1.07 (95% CI: 0.88, 1.31). PFOA levels are typically low and widespread in general populations.

The DuPont chemical plant in Washington, West Virginia, began using PFOA in its manufacturing process in 1951. The plant released PFOA into the Ohio River and air beginning in the 1950s, peaking in the 1990s, and decreasing emissions after 2001. PFOA emitted from the plant entered the groundwater, which was the public drinking water source.

In 2001, residents living near the plant filed a class action lawsuit alleging health damage due to PFOA-contaminated drinking water. A pretrial settlement required DuPont to provide funding for an independent community health study called the C8 Health Project (C8 Health Project 2012; Frisbee et al. 2009), and also resulted in the creation of the C8 Science Panel (C8 Science Panel 2012), which was tasked with determining whether there was a probable link between PFOA and disease in the community living near the plant.

The C8 Health Project surveyed Mid-Ohio Valley residents in 2005–2006. The survey collected medical history and also measured serum PFOA concentrations. The median serum PFOA concentration in this population was 28 ng/mL in 2005–2006, compared with 4 ng/mL in the United States overall (Calafat et al. 2007; Steenland et al. 2009).

Using the C8 Health Project cohort in combination with a DuPont worker cohort, the C8 Science Panel conducted subsequent interviews in 2008–2011 to gather disease incidence data. Cancer incidence results from that investigation are reported here.
Methods

Data sources and study participants. The C8 Health Project surveyed 69,030 persons between August 2005 and August 2006. Participants were eligible if they lived, worked, or attended school for ≥ 1 year in one of six contaminated water districts near the plant between 1950 and 3 December 2004. Participants reported demographic and health characteristics and an extensive residential history. Serum was collected for PFOA measurements. The estimated C8 Health Project participation rate was high (81% among current residents ≥ 20 years of age) (Frisbee et al. 2009). A detailed study description has been published previously (Frisbee et al. 2009).

The C8 Science Panel sought to enroll adult C8 Health Project participants in subsequent surveys to study disease incidence, and 74% of the participants ≥ 20 years of age consented to further contact by the C8 Science Panel. Of these, 82% participated in one or two surveys during 2008–2011. The C8 Health Project participants who completed at least one subsequent survey did not differ significantly from the original adult C8 Health Project participants with respect to age, sex, education, water district, or PFOA serum concentrations measured during 2005–2006. They reported demographic information, health-related behaviors, and medical history. In addition, we obtained a list of DuPont workers who formed a cohort that was originally constructed for a mortality study (Leonard et al. 2008; Steenland and Woskie 2012). This DuPont cohort was formed by DuPont and included 6,026 workers who were employed at the Washington, West Virginia, plant for ≥ 1 day between 1 January 1948 and 31 December 2002. Of these, we interviewed 4,391 workers, including 1,890 who were also enrolled in the C8 Health Project.

Figure 1 shows how the analysis cohort was compiled. The analysis included 32,254 persons ≥ 20 years of age, who participated in at least one subsequent survey and had exposure estimates.



Figure 1 – Cohort enrollment.

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All participants gave informed consent to participate, to match personal information to state cancer registries, and to release medical records to study personnel. Medical records were protected in accordance with the Health Insurance Portability and Accountability Act (HIPAA) regulation. The study was approved by the Emory University Institutional Review Board.

PFOA estimates. Cumulative PFOA serum concentration estimates were calculated retrospectively for each community participant for each year of life beginning in 1952 or the participant’s birth year, whichever was most recent, through 2011. Estimation procedure details have been published previously (Shin et al. 2011a, 2011b). Estimates were based on historical regional data including the PFOA amounts emitted by the DuPont facility, wind patterns, river flow, and groundwater flow. Exposure estimates took into account each participant’s reported residential history, drinking-water source, tap-water consumption, workplace water consumption, and a PFOA absorption, distribution, metabolism, and excretion model.

The exposure estimates for participants who had ever worked at the DuPont plant took into account occupational exposure they may have received at their specific job. Estimated serum levels over time for workers in different plant jobs were based on over 2,000 PFOA serum measurements taken over time from workers (Woskie et al. 2012). These estimates were used to create a job–exposure matrix to estimate serum levels for workers across time in different jobs and departments. After employment ended, exposure estimates decayed at a rate of 18% per year based on a presumed half-life of 3.5 years (Olsen et al. 2007). These estimates were then combined with estimated serum levels from residential exposure to contaminated drinking water. We estimated combined residential and occupational exposure for 3,713 (84%) of the interviewed workers.

Cancer data and confirmation process. Participants were asked “Have you ever been told by a doctor or other health professional that you had cancer or a malignancy of any kind?” Participants reported the cancer type and their age at diagnosis. Those reporting cancer were asked to allow us to review their medical records. For all self-reported cancers, we sought diagnosis validation though medical chart review or Ohio/West Virginia state cancer registry matching.

The Ohio state cancer registry was begun in 1992 and the West Virginia registry in 1993. If a participant who self-reported a cancer type was found in either of the state cancer registries to have that cancer, we confirmed their cancer using the registry. We also sought medical records for participants who reported cancer and who consented for us to do so. Some participants who reported cancer were not identified in the registries (possibly due to living out of state or receiving a cancer diagnosis prior to 1992) and in these cases, we used their medical records to confirm self-reported cancer. Medical records were received from doctors the participant reported were relevant to the specific condition and ranged from primary care physician records to oncologist records. We confirmed cancers if there was sufficient information in the record. This information could include mention of cancer diagnosis, treatments received, ICD-9 [International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) (National Center for Health Statistics 2006)] and ICD-10 [International Statistical Classification of Diseases and Related Health Problems, 10th Revision (World Health Organization 1992)] codes, or specific cancer- or tumor-descriptive characteristics.

Statistical analysis. Our main analyses were restricted to validated primary cancers. Participants who reported a cancer that was not validated were excluded from the specific cancer model and thus did not contribute any person-time to the model.

A proportional hazards regression model was run for each cancer type with the cancer as the outcome, time-varying cumulative PFOA serum concentration as the independent variable, and age as the time scale. Participants were followed from the age of 20 years or age in 1952 (the year after the first PFOA emissions), whichever was later, to cancer diagnosis age, last survey age, or death age (if deceased), whichever came first. Each model was adjusted for time-varying smoking, time-varying alcohol consumption, sex, education, and 5-year birth year period. We checked the proportional-hazards assumption for each model by including an exposure × age interaction, and found no violation of the proportional-hazards assumption (all interaction p-values > 0.05).

Our primary exposure metric was cumulative PFOA serum concentration (in nanograms per milliliter–years), which was calculated as the sum of all yearly serum concentration estimates up to a given age. We considered models that included the natural log of cumulative PFOA serum concentration as a continuous variable (a test for trend), and models that included categorical variables for cumulative serum concentration quartiles. The log of cumulative serum concentration consistently fit better than the linear untransformed cumulative serum concentration [based on the Akaike information criterion (AIC)], presumably because log transformation diminished the influence of relatively sparse data with very high cumulative exposure. The interpretation of the log cumulative exposure coefficient is that an increase of one unit of log cumulative exposure results in a relative risk (RR) of eβ compared with those with one unit less. We also tested for a linear trend in log RRs in categorical analyses by assigning the midpoint to each quartile and conducting a weighted linear regression of the log RRs on these midpoints.

Quartile cut points were calculated among the cumulative PFOA serum concentration estimates for the cancer-specific cases at diagnosis time. We also considered models that lagged cumulative PFOA serum concentration by 10 and 20 years in order to consider scenarios in which cancer could have been caused by exposure further in the past. Here we report the models that lagged cumulative PFOA serum concentration by 10 years. We also ran models limited to community residents who did not work at the plant in order to explore whether results were driven by the high PFOA exposure experienced by workers. Quartile cut points were recalculated for every cancer and population subgroup model.
Results

Demographic characteristics. Table 1 displays descriptive data for the 32,254 participants. Participants were, on average, 53 years of age at the time of their final survey, with male participants slightly older than female (54 years vs. 52 years). Most participants were of white race and were community residents. Eleven percent had ever worked at the DuPont plant. Female participants were more likely to have some college education than were male participants (36% of women vs. 29% of men). Participants who had ever worked at the DuPont plant were more likely to be male and older at the time of interview compared with participants without DuPont work experience (80% vs. 42% and 59 vs. 52 years of age).



Table 1 – Demographic characteristics of cohort (n = 32,254) by community and occupational groups [n(%) or mean ± SD].

View Table (HTML Version)
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Participants who had worked at the plant had higher PFOA serum levels in 2005–2006 and also had higher estimated annual PFOA serum levels compared with participants who never worked at the plant (Table 2). On average, each participant contributed 33 follow-up years after 20 years of age but estimated serum levels were low prior to 1980.



Table 2 – Measured and estimated PFOA exposure concentrations (ng/mL) in the cohort (n = 32, 254).

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Participants reported 3,589 different cancer diagnoses covering 21 cancer types; 2,507 cancer diagnoses were validated (70%). Table 3 shows the number of cancer diagnoses reported, the number with a received medical record or state cancer registry entry, and the number validated. We obtained a record to review for 88% of self-reported cancers. Reasons for nonvalidation included living in a different state, having a cancer prior to the existence of the two cancer registries, or failing to consent for medical record review. The accuracy of self-reported cancer varied by cancer site. Breast, bladder, kidney, prostate, thyroid, colorectal, lung, leukemia, and lymphoma cancers were more likely to be confirmed compared with other cancer types. Cervical cancer had a low validation rate, possibly due to participants misinterpreting abnormal pap smear results. Cancer was more often validated in DuPont worker participants compared with community residents who never worked at DuPont (75% vs. 69%) (see Supplemental Material, Table S1).



Table 3 – Number of reported and validateda primary cancer cases among the cohort (n = 32,254).

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Exposure–outcome associations. Table 4 shows adjusted proportional hazards model results for each cancer type based on validated cases only. Thyroid, kidney, and testicular cancer risk increased with an increase in the log of estimated cumulative PFOA serum concentration (Table 4); this association was statistically significant only for testicular cancer at the p = 0.05 level. The hazard ratios (HRs) and 95% CIs were similar between models where exposure was unlagged, models where exposure was lagged 10 years, and models where exposure was lagged 20 years (results not shown). The models generally fit slightly better for unlagged exposure compared with 10- and 20-year lagged exposures, as measured by AIC. Results based on all self-reported cancer cases were similar to estimates based on validated cases only (data not shown). The increase in testicular and kidney cancer risk by increasing log of estimated cumulative PFOA serum concentration was stronger in community residents compared with DuPont workers (see Supplemental Material, Table S2). However, the association between thyroid cancer risk and PFOA was positive and significant in DuPont workers but not community residents (see Supplemental Material, Table S2).



Table 4 – HRs (95% CIs) for the effect of logged estimated cumulative PFOA serum concentration on cancer risk in the cohort (n = 32,254).

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Table 5 reports proportional hazards model results for selected cancers using estimated cumulative PFOA serum concentration quartiles. Estimated RRs for kidney cancer and testicular cancer generally increased monotonically across quartiles, while the pattern across thyroid cancer quartiles was less consistent. p-Values for linear trend tests of log rate ratios across quartiles of unlagged exposures (using exposure category midpoints, and inverse variance weighting in a no-intercept linear regression model) were 0.25, 0.18, and 0.04 for thyroid, kidney, and testicular cancers, respectively. The p-values for thyroid, kidney, and testicular cancer trend tests with a 10-year lag were 0.57, 0.34, and 0.02. When stratified by occupational status, estimated RRs for thyroid cancer increased monotonically across quartiles among DuPont workers, but did not increase monotonically for kidney cancer among DuPont workers (see Supplemental Material, Table S3). Results for the worker cohort are limited by low sample size for cancers of interest.



Table 5 – HRs (95% CIs) by PFOA quartilea for thyroid, kidney, and testicular cancer cases among the cohort (n = 32,254).

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Because thyroid cancer is more common in women, perhaps reflecting different mechanisms from men, we ran separate analyses for men and women (24 and 74 cases, respectively). Results were similar in each group (data not shown).

Sensitivity analyses. We conducted several sensitivity analyses. We looked back at each participant’s residential history and estimated the time when each participant was first known to have begun living or working in one of the six contaminated water districts, excluding prior time. We then considered survival models that started each person’s time on this “qualifying date, ” excluding years before that date. These analyses resulted in slightly less person-time and slightly fewer cancer cases than original analyses; again, results were similar to reported results. HRs for a 1-unit increase in ln-transformed cumulative exposure in relation to thyroid, kidney, and testicular cancers were 1.06 (95% CI: 0.92, 1.23), 1.12 (95% CI: 0.99, 1.26), and 1.37 (95% CI: 0.99, 1.90) for unlagged exposures, and 1.02 (95% CI: 0.87, 1.19), 1.10 (95% CI: 0.98, 1.24), and 1.31 (95% CI: 0.95, 1.81) for exposures lagged by 10 years.
Discussion

We estimated associations between estimated cumulative PFOA exposures and incident cancers among a group of individuals exposed to PFOA through drinking water or work at the local DuPont chemical plant. Positive associations between PFOA and cancer were found for kidney, testicular, and thyroid cancer.

The positive exposure–response trend for kidney cancer is consistent with a previous DuPont worker mortality analysis, which indicated a positive exposure–response trend for kidney cancer deaths (Steenland and Woskie 2012). Our findings are also in agreement with an ecological study of incident cancer rates in relation to PFOA exposure levels between 1996 and 2005 in five Ohio and eight West Virginia counties (Vieira et al. 2013), which included some cancers diagnosed among participants in the present study population. They reported a significant positive association between kidney cancer and the two highest estimated PFOA serum exposure categories. Finally, the kidney was of a priori interest because studies using rats, mice, hamsters, rabbits, and chickens have shown that PFOA is distributed mainly in the kidneys, liver, and serum (Han et al. 2005; Kennedy et al. 2004; Lau et al. 2007).

Testicular cancer was of a priori interest because PFOA has been shown to induce testicular tumors in male rats (Biegel et al. 2001) and also to increase estradiol production in male rats, which may increase testicular tumor risk (Biegel et al. 2001). In the ecological study performed by Vieira et al. (2013), estimated PFOA exposures were positively associated with testicular cancer. As noted above, cases included in the ecological study would have partly overlapped with cases diagnosed in our study population.

To our knowledge, there are no reports of an association between PFOA and thyroid cancer from experimental studies of animals or observational studies of human populations. However, there is evidence that PFOA is associated with incident nonmalignant thyroid disease in this population (Winquist and Steenland 2012).

We confirmed self-reported cancers through state cancer registry matching and medical record review. Our cancer validation rates for breast, prostate, lung, and melanoma cancers are similar to those in previous studies, suggesting that breast, prostate, and lung cancers are typically reported accurately, whereas rectal cancer and melanoma of the skin may be reported less accurately (Bergmann et al. 1998; Stavrou et al. 2011). We tried to avoid these problems by grouping self-reported cases of “colon” and “rectal” cancer as “colorectal” cancer cases. Similarly, we did not evaluate non-melanoma skin cancer as an outcome and limited melanoma cases to participants confirmed for melanoma.

Community cohort participants (n = 30,431) had to be alive in 2004–2005 to participate in the C8 Health Project, and thus to be eligible for inclusion in our community cohort. Worker cohort participants who were not in the C8 Health Project (1,823) did not have to be alive in 2004–2005 to be included in the study. Nevertheless, because of difficulties in obtaining proxy respondents for deceased target cohort members at time of interview in 2008–2011, most of the participants from both cohorts were alive at the time of their interview in 2008–2011. It is possible that some potentially eligible kidney cancer cases would not have been enrolled or interviewed because they died before 2005, given that the 5-year survival rate for kidney cancer based on 2002–2008 SEER (Surveillance Epidemiology and End Results) data was only 70% (National Cancer Institute 2012). In contrast, cancers with low fatality rates, such as thyroid and testicular cancer, would not be expected to be missing from the study cohort. If cancer cases with higher exposure were more likely to die before they could be enrolled in our cohort, associations with PFOA may be biased toward the null, particularly for highly fatal cancers like pancreatic cancer and lung cancer; consequently our results must be interpreted with caution. On the other hand, associations could be biased away from the null if a disproportionate number of highly exposed cancer cases participated in the study.

This study has several other limitations. PFOA was estimated individually for each year of each participant’s life based on their self-reported residential history, DuPont PFOA emission patterns, and a PFOA absorption, distribution, metabolism, and excretion model. There is likely misclassification in exposure estimates, although we did find good agreement between model-predicted and measured serum levels in 2005–2006 among the C8 Health Project participants who had never worked at the DuPont plant (r = 0.67) (Shin et al. 2011b). Misclassification could cause bias if it was differential according to the outcomes evaluated. Nondifferential misclassification is more likely to result in bias toward the null than away from the null, but not always (Armstrong 1998; Steenland et al. 2000). Also, the cancer validation process was implemented only for those who self-reported a cancer. There could have been participants who had a history of cancer but did not report it. However, potential misclassification of cases as noncases would have a smaller impact on the analysis than misclassification of noncases as cases because the number of cases misclassified as noncases is likely small relative to the total number of noncases.
Conclusion

Previous research on PFOA and cancer has been primarily restricted to animal experiments, mortality studies of male workers with occupational exposure, and community studies of populations with low exposure levels and human studies have been limited by small numbers of cancer cases. The present study estimated RRs of incident cancers in association with cumulative PFOA exposure in a large community with a range of exposure levels. More than 2,500 validated cancers covering 21 different cancer types were included in the analysis, making it one of the largest cohorts ever used to examine PFOA and cancer. Our findings indicate that PFOA exposure was positively associated with kidney and testicular cancer in this Mid-Ohio Valley population. Because this is largely a survivor cohort, results for highly fatal cancers must be interpreted with caution.
References

Armstrong BG. 1998. Effect of measurement error on epidemiological studies of environmental and occupational exposures. Occup Environ Med 55(10):651–656.

Bergmann MM, Calle EE, Mervis CA, Miracle-McMahill HL. 1998. Validity of self-reported cancers in a prospective cohort study in comparison with data from state cancer registries. Am J Epidemiol 147(6):556–562.

Biegel LB, Hurtt ME, Frame SR, O’Connor JC, Cook JC. 2001. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Toxicol Sci 60(1):44–55.

Bonefeld-Jorgensen EC, Long M, Bossi R, Ayotte P, Asmond G, Krüger T, et al. 2011. Perfluorinated compounds are related to breast cancer risk in Greenlandic Inuit: a case control study. Environ Health 10:88; doi: 10.1186/1476-069X-10-88.

Butenhoff J, Costa G, Elcombe C, Farrar D, Hansen K, Iwai H, et al. 2002. Toxicity of ammonium perfluorooctanoate in male cynomolgus monkeys after oral dosing for 6 months. Toxicol Sci 69(1):244–257.

C8 Health Project. 2012. C8 Health Project Homepage. Available: http://publichealth.hsc.wvu.edu/c8/ [accessed 5 February 2013].

C8 Science Panel. 2012. C8 Science Panel Homepage. Available: http://www.c8sciencepanel.org/index.html [accessed 5 February 2013].

Calafat AM, Wong LY, Kuklenyik Z, Reidy JA, Needham LL. 2007. Polyfluoroalkyl chemicals in the U.S. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003–2004 and comparisons with NHANES 1999–2000. Environ Health Perspect 115:1596–1602; doi: 10.1289/ehp.10598.

DeWitt JC, Shnyra A, Badr MZ, Loveless SE, Hoban D, Frame SR, et al. 2009. Immunotoxicity of perfluorooctanoic acid and perfluorooctane sulfonate and the role of peroxisome proliferator-activated receptor alpha. Crit Rev Toxicol 39(1):76–94.

Eriksen KT, Sørensen M, McLaughlin JK, Lipworth L, Tiønneland A, Overvad K, et al. 2009. Perfluorooctanoate and perfluorooctanesulfonate plasma levels and risk of cancer in the general Danish population. J Natl Cancer Inst 101(8):605–609.

Frisbee SJ, Brooks AP, Maher A, Flensborg P, Arnold S, Fletcher T, et al. 2009. The C8 Health Project: design, methods, and participants. Environ Health Perspect 117:1873–1882; doi: 10.1289/ehp.0800379.

Han X, Kemper RA, Jepson GW. 2005. Subcellular distribution and protein binding of perfluorooctanoic acid in rat liver and kidney. Drug Chem Toxicol 28(2):197–209.

Kennedy G, Butenhoff J, Olsen G, O’Connor JC, Seacat AM, Perkins RG, et al. 2004. The toxicology of perfluorooctanoate. Crit Rev Toxicol 34(4):351–384.

Koeffler HP. 2003. Peroxisome proliferator-activated receptor γ and cancers. Clin Cancer Res. 9(1):1–9.

Lau C, Anitole K, Hodes C, Lai D, Pfahles-Hutchens A, Seed J. 2007. Perfluoroalkyl acids: a review of monitoring and toxicological findings. Toxicol Sci 99(2):366–394.

Leonard RC, Kreckmann KH, Sakr CJ, Symons JM. 2008. Retrospective cohort mortality study of workers in a polymer production plant including a reference population of regional workers. Ann Epidemiol 18(1):15–22.

Lundin JI, Alexander BH, Olsen GW, Church TR. 2009. Ammonium perfluorooctanoate production and occupational mortality. Epidemiology 20(6):921–928.

National Cancer Institute. 2012. Surveillance Epidemiology and End Results. SEER Stat Fact Sheets: Kidney and Renal Pelvis Cancer. Available: http://seer.cancer.gov/statfacts/html/ki​drp.html#survival [accessed 5 February 2013].

National Center for Health Statistics. 2006. International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM). Available: http://www.cdc.gov/nchs/icd/icd9cm.htm [accessed 16 September 2013].

Olsen GW, Burris J, Ehresman D, Froehlich JW, Seacat AM, Butenhoff JL, et al. 2007. Half-life of serum elimination of perfluorooctanesulfonate, perluorohexanesulfonate, and perefluorooctanoate in retired fluorochemical production workers. Environ Health Perspect 115:1298–1365; doi: 10.1289/ehp.10009.

Seals R, Bartell SM, Steenland K. 2011. Accumulation and clearance of perfluorooctanoic acid (PFOA) in current and former residents of an exposed community. Environ Health Perspect 119:119–124; doi: 10.1289/ehp.1002346.

Shin HM, Vieira VM, Ryan PB, Detwiler R, Sanders B, Steenland K, et al. 2011a. Environmental fate and transport modeling for perfluorooctanoic acid emitted from the Washington Works facility in West Virginia. Environ Sci Technol 45(4):1435–1442.

Shin HM, Vieira VM, Ryan PB, Steenland K, Bartell SM. 2011b. Retrospective exposure estimation and predicted versus observed serum perfluorooctanoic acid concentrations for participants in the C8 Health Project. Environ Health Perspect 119:1760–1765; doi: 10.1289/ehp.1103729.

Stavrou E, Vajdic CM, Loxton D, Pearson S. 2011. The validity of self-reported cancer diagnoses and factors associated with accurate reporting in a cohort of older Australian women. Cancer Epidemiol 35(6):e75–e80.

Steenland K, Deddens JA, Zhao S. 2000. Biases in estimating the effect of cumulative exposure in log-linear models when estimated exposure levels are assigned. Scand J Work Environ Health 26(1):37–43.

Steenland K, Fletcher T, Savitz DA. 2010. Epidemiologic evidence on the health effects of perfluorooctanoic acid (PFOA). Environ Health Perspect 118:1100–1108; doi: 10.1289/ehp.0901827.

Steenland K, Jin C, MacNeil J, Lally C, Ducatman A, Vieira V, et al. 2009. Predictors of PFOA levels in a community surrounding a chemical plant. Environ Health Perspect 117:1083–1088; doi: 10.1289/ehp.0800294.

Steenland K, Woskie S. 2012. Cohort mortality study of workers exposed to perfluorooctanoic acid. Am J Epidemiol 176(10):909–917.

Suchanek KM, May FJ, Robinson JA, Lee WJ, Holman NA, Monteith GR, et al. 2002. Peroxisome proliferator-activated receptor α in the human breast cancer cell lines MCF-7 and MDA-MB-231. Mol Carcinog 34(4):165–171.

U.S. Environmental Protection Agency. 2005. Draft Risk Assessment of the Potential Human Health Effects Associated with Exposure to Perfluoroctanoic Acid and Its Salts. Available: http://www.epa.gov/oppt/pfoa/pubs/pfoari​sk.pdf [accessed 5 February 2013].

U.S. Environmental Protection Agency. 2006. Advisory Board Review of EPA’s Draft Risk Assessment of Potential Human Health Effects Associated with PFOA and Its Salts. EPA-SAB-06-006. Available: http://yosemite.epa.gov/sab/sabproduct.n​sf/A3C83648E77252828525717F004B9099/$Fil​e/sab_06_006.pdf [accessed 5 February 2013].

Vieira VM, Hoffman K, Shin H-M, Weinberg JM, Webster TF, Fletcher T. 2013. Perfluorooctanoic acid exposure and cancer outcomes in a contaminated community: a geographic analysis. Environ Health Perspect 121:318–323; doi: 10.1289/ehp.1205829.

Winquist A, Steenland K. 2012. Association between cumulative PFOA exposure and thyroid disease in community and worker cohorts [Abstract]. Epidemiology 23(5S):S121.

World Health Organization. 1992. International Statistical Classification of Diseases and Related Health Problems, 10th Revision. Geneva:WHO. Available: http://apps.who.int/classifications/icd1​0/browse/2010/en [accessed 16 September 2013].

Woskie SR, Gore R, Steenland K. 2012. Retrospective exposure assessment of perfluorooctanoic acid serum concentrations at a fluoropolymer manufacturing plant. Ann Occup Hyg Apr 26:1–13.

EPA and DOJ announce settlement with Par Hawaii Refining for Clean Air Act violations at Kapolei Refinery

EPA and DOJ announce settlement with Par Hawaii Refining for Clean Air Act violations at Kapolei Refinery
Part of $425 million settlement with co-defendant Tesoro covering six refineries
07/18/2016
Contact Information:
Dean Higuchi (higuchi.dean@epa.gov)
808-541-2711

SAN FRANCISCO – The U.S. Environmental Protection Agency (EPA) and the U.S. Department of Justice today announced a settlement with Par Hawaii Refining for alleged Clean Air Act violations at its Kapolei Refinery, in Kapolei, Hawaii, as part of a larger $425 million settlement covering six refineries.

Par Hawaii will spend an estimated $47 million to install and operate pollution control equipment at the Kapolei Refinery, formerly owned by the Tesoro Corp.

“EPA remains committed to ensuring companies take responsibility for protecting public health and the environment,” said Alexis Strauss, EPA’s Acting Regional Administrator for the Pacific Southwest. “With this agreement, Par Hawaii will not only reduce harmful emissions from refinery leaks and flares, but will also reduce emissions of nitrogen oxides by nearly 240 tons per year from the Kapolei refinery heaters and boilers.”

Under the settlement, Par Hawaii and subsidiaries of Tesoro Corp. will spend about $403 million to install and operate pollution control equipment at refineries in Alaska, California, Hawaii, North Dakota, Utah, and Washington State. Tesoro will also pay a civil penalty of $10.45 million, of which the United States will receive $8.05 million. Co-plaintiffs Alaska, Hawaii, and Washington State’s Northwest Clean Air Agency will split the remainder, receiving $1.3 million, $850,000, and $250,000, respectively. Tesoro will also spend about $12.2 million to fund projects that will improve public health in local communities previously impacted by pollution.

Once implemented, the pollution controls required by the settlement will reduce annual emissions at the six refineries by an estimated 773 tons of sulfur dioxide, 407 tons of nitrogen oxides, 1,140 tons of volatile organic compounds, 27 tons of hazardous air pollutants, 20 tons of hydrogen sulfide and the equivalent of 47,034 tons of carbon dioxide.

Tesoro Corp., is headquartered in San Antonio, Texas and its subsidiaries, Tesoro Alaska Company LLC, Tesoro Logistics L.P., and Tesoro Refining & Marketing Company LLC operate five of the refineries covered by this settlement. Par Pacific Holdings, Inc., formerly known as Par Petroleum Corp. and a parent corporation of Par Hawaii Refining, purchased the Kapolei, Hawaii refinery from Tesoro in 2013.

The penalty is due 30 days after the consent decree is entered by the court. There will be a 30 day public comment period on the consent decree lodged today. Information on how to comment on the consent decree is available on the Department of Justice’s website.

For more information on the settlement or to read the consent decree, go to https://www.epa.gov/enforcement/tesoro-and-par-clean-air-act-settlement

EPA, Goodrum Farm CR314, LLC Reach Settlement on Clean Water Act Violations

EPA, Goodrum Farm CR314, LLC Reach Settlement on Clean Water Act Violations
07/18/2016
Contact Information:
Mark Hanson (hanson.mark@epa.gov)
913-551-7788

Environmental News

FOR IMMEDIATE RELEASE

(Lenexa, Kan., July 18, 2016) - EPA Region 7 has reached a proposed administrative settlement with Goodrum Farm CR314, LLC, in Butler County, Mo., to resolve violations of Section 404 of the Clean Water Act (CWA). As part of the settlement, the company has agreed to pay a civil penalty of $15,000.

During a July 16, 2014, inspection, U.S. Army Corps of Engineers (USACE) inspectors found the company had placed dredged and fill material into forested wetlands, in an effort to convert the wetlands to agricultural cropland. This resulted in the unauthorized impact of approximately 9.46 acres of wetlands adjacent to a designated “water of the United States.”

Under a previously issued administrative compliance order to address the CWA violations, Goodrum Farm CR314, LLC, mitigated the impacted wetland acres by placing approximately 35 acres of the property into a conservation easement, preventing further development, including future farming.

Under this proposed settlement, Goodrum Farm CR314, LLC, will pay a $15,000 penalty for its alleged Section 404 CWA violations.

Unpermitted destruction of wetland areas can create numerous environmental impacts, including degradation of watershed health, habitat loss, impacts to stream channel configuration, and decreased biological diversity. Wetland degradation also impedes a wetland’s abilities to absorb floodwaters and filter pollutants. Prior to conducting activities that may impact wetlands, streams, or rivers, landowners should consult with the USACE to determine if the planned activity is authorized under Section 404 of the CWA.

The Clean Water Act seeks to protect streams and wetlands that form the foundation of the nation’s water resources. Protecting streams and wetlands is also part of adapting to climate change impacts like drought, stronger storms, and warmer temperatures.

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EPA Issues Stop-Sale Order to PuriCore, Inc. To Protect Public from Unregistered Pesticide in Supermarkets

EPA Issues Stop-Sale Order to PuriCore, Inc. To Protect Public from Unregistered Pesticide in Supermarkets
07/18/2016
Contact Information:
Roy Seneca (seneca.roy@epa.gov)
(215) 814-5567

PHILADELPHIA (July 18, 2016) – PuriCore Inc. of Malvern, Pa. has paid a $550,000 penalty for the unauthorized distribution of two pesticide products that were used in supermarkets nationwide, the U.S. Environmental Protection Agency announced today.

The products included ProduceFresh, an unregistered pesticide used as part of a crisping process in the produce section of stores, and FloraFresh that was used in floral departments.

Along with the penalty, EPA issued a stop-sale order to PuriCore Inc. prohibiting the sale of ProduceFresh.

The order and penalty were issued under the Federal Insecticide, Fungicide and Rodenticide Act (FIFRA), the federal statute regulating the manufacture, labeling, sale, and use of pesticide products. FIFRA's safeguards protect public health and the environment by ensuring the safe production and handling of pesticides and devices; and by preventing false, misleading, or unverifiable product claims.

Although PuriCore has submitted an application to EPA to register ProduceFresh as a pesticide, EPA has not completed its review of the risks associated with the product. No stop-order was issued for FloraFresh because it was registered as a pesticide as of Feb. 12. However, PuriCore had been distributing FloraFresh to supermarkets for at a least a year prior to it being registered.

For more information about EPA’s pesticide program, visit www.epa.gov/pesticides .

EPA and DOJ announce settlement with Tesoro for Clean Air Act violations at Martinez Refinery. Part of $425 million settlement covering six refineries

EPA and DOJ announce settlement with Tesoro for Clean Air Act violations at Martinez Refinery.  Part of $425 million settlement covering six refineries
07/18/2016
Contact Information:
Dean Higuchi (higuchi.dean@epa.gov)
808-541-2711

SAN FRANCISCO – The U.S. Environmental Protection Agency (EPA) and the U.S. Department of Justice today announced a settlement with Tesoro Refining and Marketing Co. (Tesoro) for alleged Clean Air Act violations at its Martinez Refinery, in Martinez, California, as part of a larger $425 million settlement covering six refineries.

Tesoro will spend an estimated $24 million to install and operate pollution control equipment at the Martinez Refinery and $1 million to fund the replacement of old diesel school buses in Contra Costa County with at least four new compressed natural gas school buses. Replacing the school buses will help decrease emissions of nitrogen oxides, sulfur dioxides, particulate matter, greenhouse gases, and other air pollutants in an area designated nonattainment for the federal ozone air quality standard.

“EPA remains committed to ensuring companies take responsibility for protecting public health and the environment,” said Alexis Strauss, EPA’s Acting Regional Administrator for the Pacific Southwest. “With this agreement, Tesoro will not only reduce harmful emissions from its coker and flares, but will also reduce sulfur dioxide emissions by nearly 190 tons per year from the Martinez refinery acid plant.”

Under the settlement, Tesoro and related companies, and Par Hawaii Refining will spend about $403 million to install and operate pollution control equipment at refineries in Alaska, California, Hawaii, North Dakota, Utah, and Washington State. Tesoro will also pay a civil penalty of $10.45 million, of which the United States will receive $8.05 million. Co-plaintiffs Alaska, Hawaii, and Washington State’s Northwest Clean Air Agency, will split the remainder, receiving $1.3 million, $850,000, and $250,000, respectively. Tesoro will also spend about $12.2 million to fund projects that will improve public health in local communities previously impacted by pollution.

Once implemented, the pollution controls required by the settlement will reduce annual emissions at the six refineries by an estimated 773 tons of sulfur dioxide, 407 tons of nitrogen oxides, 1,140 tons of volatile organic compounds, 27 tons of hazardous air pollutants, 20 tons of hydrogen sulfide and the equivalent of 47,034 tons of carbon dioxide.

Tesoro Corp., is headquartered in San Antonio, Texas and its subsidiaries, Tesoro Alaska Company LLC, Tesoro Logistics L.P., and Tesoro Refining & Marketing Company LLC operate five of the refineries covered by this settlement. Par Pacific Holdings, Inc., formerly known as Par Petroleum Corp. and a parent corporation of Par Hawaii Refining, purchased the Kapolei, Hawaii refinery from Tesoro in 2013.

The penalty is due 30 days after the consent decree is entered by the court. There will be a 30 day public comment period on the consent decree lodged today. Information on how to comment on the consent decree is available on the Department of Justice’s website.

For more information on the settlement or to read the consent decree, go to https://www.epa.gov/enforcement/tesoro-and-par-clean-air-act-settlement

OIL REFINERS TO REDUCE AIR POLLUTION AT SIX REFINERIES UNDER SETTLEMENT WITH EPA AND DEPARTMENT OF JUSTICE

OIL REFINERS TO REDUCE AIR POLLUTION AT SIX REFINERIES UNDER SETTLEMENT WITH EPA AND DEPARTMENT OF JUSTICE
07/18/2016
Contact Information:
Julia P. Valentine (valentine.julia@epa.gov)
(202) 564-2663, (202) 564-4355 WASHINGTON—The U.S. Environmental Protection Agency (EPA) and the U.S. Department of Justice today announced a $425 million settlement with subsidiaries of Tesoro Corp., and Par Hawaii Refining that resolves alleged Clean Air Act violations and protects public health by reducing air pollution at six refineries. Under the settlement, the two companies will spend about $403 million to install and operate pollution control equipment, and Tesoro will spend about $12 million to fund environmental projects in local communities previously impacted by pollution. Tesoro will also pay a $10.45 million civil penalty.

“The advanced technologies Tesoro and Par are required to implement are the future for protecting people from toxic air emissions,” said Cynthia Giles, EPA Assistant Administrator for Enforcement and Compliance Assurance. "This settlement puts new enforcement ideas to work that will dramatically cut pollution and protect communities."

“This settlement, achieved in partnership with states, will benefit the air quality in communities across the Western United States,” said Assistant Attorney General John C. Cruden for the Justice Department’s Environment and Natural Resources Division. “It uses cutting edge technology to address global environmental issues like climate change by controlling flaring and provides important reductions of harmful air pollution in communities facing environmental and health challenges.”

Today’s settlement, a consent decree lodged in U.S. District Court for the Western District of Texas, includes provisions that resolves ongoing Clean Air Act violations at refineries in Kenai, Alaska; Martinez, California; Kapolei, Hawaii; Mandan, North Dakota; Salt Lake City, Utah; and Anacortes, Washington. Of the $10.45 million civil penalty that Tesoro will pay, the United States will receive $8,050,000, and co-plaintiffs including the states of Alaska and Hawaii, and the Northwest Clean Air Agency will share $2.4 million.

Once the companies install the pollution controls required by the settlement, annual emissions reductions at the six refineries will total an estimated 773 tons of sulfur dioxide, 407 tons of nitrogen oxides, 1,140 tons of volatile organic compounds, 27 tons of hazardous air pollutants, 20 tons of hydrogen sulfide and the equivalent of 47,034 tons of carbon dioxide, which is a greenhouse gas. A large number of the emissions reductions will occur in areas with impaired air quality and protect populations at risk for respiratory illnesses. In particular, this settlement will reduce greenhouse gas emissions from flaring at the subject refineries by over 60 percent.

The settlement addresses a range of alleged leak detection and repair and flaring violations under the Clean Air Act at all six refineries as well as violations of the Act’s Prevention of Significant Deterioration, Non-Attainment New Source Review, New Source Performance Standards and National Emission Standards for Hazardous Air Pollutants at certain refineries. The settlement also addresses various violations of state clean air laws, programs and permits.

Refineries process crude oil into products like gasoline, diesel fuel, kerosene, jet fuel, asphalt and liquefied petroleum gas and emit pollutants from a number of different sources. At the refineries subject to this settlement, fluid catalytic cracking units, sulfuric acid plants, heaters, boilers and sulfur recovery units, are substantial emitters of nitrogen oxides (NOx) and sulfur dioxide (SO2). Flaring results in emissions of SO2, greenhouse gases and toxic air pollutants, including volatile organic compounds (VOCs) and hazardous air pollutants. Fugitive emissions of VOCs result from leaking valves and pumps and can result in numerous health effects, including eye, nose and throat irritation, headaches, loss of coordination, nausea and damage to liver, kidney and the central nervous system, among other effects.

Leaks, flares, and excess emissions from refineries emit hazardous air pollutants, or air toxics, that are known or suspected to cause cancer, birth defects, and seriously impact the environment. SO2 and NOx have numerous adverse effects on human health and are significant contributors to acid rain, smog and haze. Refineries also emit greenhouse gases that contribute to climate change, as well as fugitive VOCs.

The settlement incorporates the latest technological approaches to reducing flaring and making the flaring that does occur as efficient as possible. And in addition to installing pollution control equipment, the settlement requires Tesoro to use a series of state-of-the-art Next Generation Compliance tools to monitor pollution. Tesoro will use infrared gas-imaging cameras at four refineries to supplement the company’s enhanced leak detection and repair program. These cameras are able to locate fugitive VOC emissions that may not be otherwise detected and to address these fugitive emissions and in doing so protect refinery employees from them. Tesoro will also pay for third-party auditing of compliance with the enhanced leak detection and repair requirements at all six facilities. EPA’s Next Generation Compliance strategy works to advance the use of state-of-the-art technology to identify and reduce pollution.

Under the settlement, Tesoro will also spend about $12.2 million to fund three pollution mitigation projects. In addition to installing infrared cameras, Tesoro will install ultra-low NOx burners on a furnace at its Salt Lake City refinery. Tesoro estimates that the cost of this mitigation project is $10.8 million and is expected to result in significant quantifiable reductions in NOX emissions. Tesoro will also contribute $1 million to fund the replacement of old diesel school buses in Contra Costa County, California, with new compressed natural gas (CNG) school buses.

Replacing existing school buses that run on diesel with vehicles that are powered by CNG decreases emissions of NOX, SO2, PM, greenhouse gases and other air pollutants.This settlement is part of EPA’s National Enforcement Initiative to control harmful emissions from large sources of pollution, which includes refineries, under the Clean Air Act’s Prevention of Significant Deterioration requirements. The total combined SO2 and NOx emission reductions secured from all settlements under this initiative will exceed 2 million tons each year once all the required pollution controls have been installed and implemented.

Tesoro Corp., is headquartered in San Antonio, Texas, and its subsidiaries, Tesoro Alaska Company LLC, Tesoro Logistics L.P. and Tesoro Refining & Marketing Company LLC operate five of the refineries covered by this settlement. Par Pacific Holdings, Inc., formerly known as Par Petroleum Corp. and a parent corporation of Par Hawaii Refining, purchased the Kapolei refinery from Tesoro in 2013.

There will be a 30 day public comment period on the consent decree lodged today. Information on how to comment on the consent decree will be available in the Federal Register and on the Department of Justice’s website: www.justice.gov/enrd/consent-decrees.

For more information on the settlement or to read the consent decree, go to https://www.epa.gov/enforcement/tesoro-and-par-clean-air-act-settlement

Two people killed and two others injured in a two-vehicle head-on collision in Folsom, California

 

2 killed in 2-vehicle crash near Folsom Dam
Deadly crash shut down Folsom Lake Crossing in both directions
UPDATED 7:14 AM PDT Jul 18, 2016 

 FOLSOM, Calif. (KCRA) —Two people were killed and two others were hurt Sunday evening in a two-vehicle crash that shut down a Folsom roadway for several hours, police said.
 
The crash happened about 5:10 p.m. on Folsom Lake Crossing when a vehicle traveling west crossed over into the eastbound lanes and hit another vehicle, according to Folsom police.

Two people inside the vehicle that crossed over into oncoming traffic were killed, while two people in the vehicle going east were taken to a hospital, police said. The extent of their injuries were not given.

Speed appears to be factor in the crash, investigators said.

Folsom Lake Crossing was closed in both directions but has since reopened.

No information has been released.

Speeding and drunk ATV driver loses his life west of Watts, OK

OKLAHOMA CITY (AP) - Authorities are investigating after a 48-year-old Arkansas man died in an ATV crash in eastern Oklahoma.


The Oklahoma Highway Patrol says the incident happened Saturday about 10:30 p.m. about seven miles west of Watts.

A patrol report indicates that the driver, Keith Baker of Russellville, Arkansas, was headed north on a private property trail when, for some unknown reason, his vehicle overturned and came to a rest.

The victim was pronounced dead at the scene.

A field report by the trooper indicates the odor of alcohol near the victim and cites unsafe speed on a curve or turn as a cause of the collision.

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