The topic for this unit was the classification of carcinogens by the International Agency for Research on Cancer (IARC). For this assignment, pick a group 1 carcinogen from the IARC. Find at least five peer-reviewed journal articles that support the relationship between the carcinogen and the cancer that it causes.

Some suggested topics might be

 benzene and leukemia,

 crystalline silica dust and lung cancer, or

 vinyl chloride and liver cancer.

The Business Source Complete database is a good source of journals for safety-related articles from the CSU Online Library. The Literature Review must include the following components:

 an introduction of your topic of choice (include some background information on the origins of exposure and cancer),

 the methods used to search for the articles,

 the results of the articles,

 a discussion and conclusion with your own opinion, and.

 APA references and in-text citations for the article.

The literature review must be three to four pages in length and follow APA formatting.

References

Sahmel, J., Unice, K., Scott, P., Cowan, D., & Paustenbach, D. (2009). The Use of Multizone Models to Estimate an Airborne Chemical Contaminant Generation and Decay Profile: Occupational Exposures of Hairdressers to Vinyl Chloride in Hairspray During the 1960s and 1970s. Risk Analysis: An International Journal, 29(12), 1699-1725. doi:10.1111/j.1539-6924.2009.01311.x

COHRSSEN, J. J., & MILLER, H. I. (2015). STUNTED HARVEST. Regulation, 38(4), 22-25.

Occupational Exposure to Respirable Crystalline Silica. (cover story). (2017). Industrial Safety & Hygiene News, 51(1), 45.

2017 top standards

History OSHA’s standards for welding, cutting and brazing

in general industry and construction were based on the 1967 ANSI standard Z49.1.

Why this standard is important Welding, cutting and brazing are hazardous activities

that pose a unique combination of both safety and health risks to more than 500,000 workers in a wide variety of industries. The risk from fatal injuries alone is more than four deaths per thousand workers over a working lifetime.

Hazards Health hazards from welding, cutting, and brazing

operations include exposures to metal fumes and to UV radiation. Safety hazards from these operations include burns, eye damage, electrical shock, cuts, and crushed toes and fingers. Many of these can be controlled with proper work practices and PPE.

Enforcement Statistics: October 2015 through September 2016 – totals for

all industries Citations: 145 Inspections: 119 Penalty: $369,553

Most Frequently Cited Provisions

• If the object to be welded or cut cannot be moved and if all the fire hazards cannot be removed, then guards shall be used to confine the heat, sparks, and slag, and to protect the immovable fire hazards.

• Wherever there are floor openings or cracks in the flooring that cannot be closed, precautions shall be taken

so that no readily combustible materials on the floor below will be exposed to sparks which might drop through the floor. The same precautions shall be observed with regard to cracks or holes in walls, open doorways and open or broken windows.

• When arc welding is to be sus- pended for any substantial period of time, such as during lunch or over- night, all electrodes shall be removed from the holders and the holders care- fully located so that accidental contact cannot occur and the machine be disconnected from the power source.

Most cited industries 1 Fabricated Metal Product Manufacturing 2 Machinery Manufacturing 3 Transportation Equipment Manufacturing 4 Electrical Equipment, Appliance, and Component

Manufacturing 5 Merchant Wholesalers, Durable Goods 6 Specialty Trade Contractors 7 Primary Metal Manufacturing 8 Support Activities for Mining 9 Motor Vehicle and Parts Dealers 10 Miscellaneous Manufacturing

What must employers do to protect employees?

Welders should understand the hazards of the materials they are working with. OSHA’s Hazard Communication standard requires employers to provide information and train- ing for workers on hazardous materials in the workplace. Welding surfaces should be cleaned of any coating that could

potentially create toxic exposure, such as solvent residue and paint. Workers should be positioned to avoid breathing weld- ing fume and gases. For protection from radiant energy, workers must use PPE, such as safety glasses, goggles, welding helmets or welding face shields.

Key Letter of Interpretation

OSHA’s welding, cutting, and braz- ing standard, 29 C.F.R. §1910.252(b)

(3), outlines specific PPE requirements for welders. This provision states that employees exposed to the hazards created by welding, cutting, or brazing operations must be protected by PPE in accordance with the require- ments of the general personal protective equipment standard, §1910.132. The welding standard also states that “[a]ppropriate protective clothing required for any welding will vary with the size, nature and location of the work to be performed.” Therefore, if welders are exposed to flash fires or short-duration flame exposures, OSHA expects that employers would provide and ensure the use of FRC to protect workers from these hazards.

Compliance Assistance Eye Protection against Radiant

Energy during Welding and Cutting in Shipyard Employment. OSHA Fact Sheet, (2012, January). Discusses protection from radiant energy and the requirements for workers to use per- sonal protective equipment.

Controlling Hazardous Fume and Gases during Welding. OSHA Fact Sheet FS-3647, (2013).

Welding, Cutting and Brazing 1910.252

History The U.S. Department of Labor became aware of the

dangers of respirable crystalline silica in the 1930s, but it wasn’t until 1971 that silica exposure standards were set by the newly-established OSHA. The final rule issued on March 25, 2016 is comprised of two standards, one for Construction and one for General Industry and Maritime.

Why this standard is important An estimated 2.3 million workers are exposed to

respirable crystalline silica in their workplaces, pri- marily in construction, general industry and hydraulic fracturing. Exposure can occur during the drilling, cutting, crushing, or grinding of silica-containing materials such as concrete and stone and during brick manufacturing and foundry operations.

Hazards When inhaled, the very small respirable particles in

silica dust can penetrate deep into the lungs and cause disabling and sometimes fatal lung diseases such as silicosis and lung cancer, as well as kidney disease.

Enforcement Statistics Because the rule was issued this year, there are no

enforcement statistics available yet.

Key Provisions • Reduces the permissible exposure limit (PEL) for

respirable crystalline silica to 50 micrograms per cubic meter of air, averaged over an 8-hour shift.

• Requires employers to use engineering controls to limit worker exposure; provide respirators when engineering controls cannot adequately limit exposure; limit worker access to high exposure areas; offer medi- cal exams to highly exposed workers, and train work- ers on silica risks and how to limit exposures.

Industries that may be cited Crystalline silica exposure can occur in following

industries and operations: 1. Construction 2. Glass products 3. Structural clay products 4. Concrete products 5. Foundries 6. Paintings and coatings 7. Refractory products 8. Cut stone and stone products 9. Hydraulic fracturing for gas and oil 10. Maritime work

What must employers do to protect employees?

• Where possible, silica should be eliminated or substituted with a safer option.

• Engineering controls should then be considered, such as using local exhaust ventilation, using con-

tainment methods (e.g., blast-cleaning machines and cabinets), and wet sawing or wet drilling of silica- containing materials.

• Administrative or work practice controls may include limiting workers’ exposure time and requir- ing workers to shower and change into clean clothes before leaving a worksite.

• Personal protection equipment such as proper respiratory protection may be used to keep workers’ exposure below the OSHA PEL.

Respirable Crystalline Silica Compliance Directive:

Directive number: CPL 03-00-007 Compliance date: January 24, 2008 Subject: National Emphasis Program – Crystalline

Silica

Compliance Assistance: Crystalline Silica Exposure in General

Industry. This OSHA Health Hazard Information Card provides good work practices for workers.

A Guide to Working Safely With Silica: If It’s Silica, It’s Not Just Dust. This NIOSH guide provides information about the health hazards of silica and suggests ways to prevent silicosis.

Occupational Exposure to Respirable Crystalline Silica Construction standard: 1926.1153 General industry/maritime standard: 1910.1053

01p45Standards WeldingSilica.indd 45 12/21/16 7:48 PM

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22 | NEW REPUBLIC

THE THINGS THEY

BURNED A private contractor tossed U.S. military waste in Iraq and

Afghanistan into giant pits and burned it. Now soldiers forced to breathe the toxic fumes are sick or dying—and the government is using faulty science to evade responsibility.

BY JENNIFER PERCY

PHOTOGRAPHS BY NINA BERMAN

DECEMBER 2016 | 23

Specialist Nicolas Plantiko burned dogs. Sergeant Thomas J. Brennan burned lithium ion batteries, flame-resistant frog suits, and MK-19 rounds. He burned plastic chemical drums, nylon, tires, wires, and tarps. He burned shit and piss. Sergeant Bill Moody’s unit burned a Porta-John, dried-up MREs, and 500 loaves of moldy bread. Staff Sergeant Louis Levesque burned bunk beds. Private Johnnie Stevenson burned plastic bottles because he loved the way they hissed. Airborne infantryman Dennis St. Pierre burned radio batteries and chemlights. Sergeant Carlos Castro joked about burning another soldier for talking too much. Captain Matthew Frye burned a packet of Tabasco sauce that exploded and nearly took out the jtac’s eye. Staff Sergeant Tim Wymore burned 25 loads of deet-soaked tents and walked around with the taste of smoke in his mouth. Sergeant Zachary Bell burned batteries because the Taliban used the carbon rods for IED triggers. Specialist Dante Sowell burned burlap bags so he wouldn’t have to fill them up with sand. Captain Adrian Bonenberger watched a Christmas tree go into a burn pit. Private George Snyder burned Private Stuart Decker’s one confirmed kill. Sergeant Casey Rohrich burned a human toe. They burned magazines, movies, junk food, college brochures, and pamphlets for the GI Bill. They burned amputated body parts and Humvee parts. They burned human waste and

plastic meal trays. They burned the blood and clothes of the wounded.

Everything—all the trash of the war—was thrown in a burn pit, soaked with jet fuel, and torched. There were hundreds of open-air garbage dumps, spread out across Afghanistan and Iraq, right next to encampments where American soldiers lived and worked, ate and slept. The pits burned day and night, many of them around the clock, seven days a week. There were backyard-size pits lit by patrols of a few dozen men, and massive, industrial-size pits designed to incinerate the endless stream of waste produced by U.S. military bases. Camp Speicher, in Iraq, produced so much trash that it had to operate seven burn pits simultaneously. At the height of the surge, according to the Military Times, Joint Base Balad was churning out three times more garbage than Juneau, Alaska, which had a comparable population. Balad’s pit, situated in the northwest corner of the base, spanned ten acres and burned more than 200 tons of trash a day.

Much of the waste in the pits was toxic, and burning it released a lethal array of pollutants: particulate matter, volatile organic compounds, hydrocarbons, neurotoxins. JP-8, the jet fuel often used to ignite trash, released clouds of benzene, a known carcinogen. One analysis conducted on dust

The scarred lungs of a veteran exposed to a burn pit in Iraq. He’s been diagnosed with constrictive bronchiolitis, an often fatal lung disease.

samples from Camp Victory in Iraq found hazardous levels of copper, iron, and titanium particles. Other researchers detected dioxin, the cancer-causing chemical found in Agent Orange. Burning plastic bottles released dioxin and hydrochloric acid, and burning foam cups released dioxin, benzene, and other carcinogens.

“Ash spread over everything,” Leon Russell Keith, a military contractor who was stationed at Balad, testified at a Senate hearing in 2009. “Our beds, our clothing, the floor.” Thick black smoke poured into the barracks. The air conditioners blew ash. Ash stained the bed sheets. Their teeth turned black from the soot. Ash rained down on the men, on the American troops, the Iraqi detainees, the Iraqi correctional officers. One soldier described the smoke as thick “like San Francisco fog.” Another called it “pollen dust.” The color of the smoke changed depending on what was burning that day. It could be blue and black, or yellow and orange. Mostly it was black. Everyone inhaled it. They ingested it. It was on their skin.

The burn pits were supposed to be temporary, an imperfect stopgap required by the exigencies of invasion and occupation. But like much of the war, the burn pits were privatized, the military’s trash turned into a lucrative, for-profit enterprise. Kellogg Brown & Root, which operated the burn pits as part of a $35 billion logistics contract in Afghanistan and Iraq, went on burning waste in open-air pits for years, even after the government dispatched cleaner- burning incinerators to U.S. bases. The military was aware that the burn pits posed a risk to soldiers. “There is an acute health hazard for individuals,” an Air Force bioenvironmental engineer warned his superiors in 2006.

It didn’t take long for soldiers to begin to fall ill. As early as 2004, veterans who had served near burn pits began complaining of a complex and enigmatic constellation of symptoms: asthma, sinusitis, bronchitis, unexplained diarrhea, persistent runny nose or cough, severe headaches and abdominal pain, ulcers, weeping lesions on the extremities, chronic infections. Many coughed up black mucus, which they called “plume crud,” “black goop,” or “Iraqi crud.” Some developed cancers—tumors grew on their lungs, brains, bone, and skin—including leukemia. Others suffered from severe respiratory conditions, including chronic obstructive pulmonary disease and constrictive bronchiolitis, a rare and often fatal lung disorder for which there is no treatment.

Rick Lamberth, an Army Reserve lieutenant colonel, worked for Kellogg Brown & Root in Iraq and Afghanistan from 2003 to 2009. Lamberth suffers from rashes, spits up bloody mucus, and has shortness of breath. Shortly after returning home, he testified to a panel of Democratic senators about how KBR operated the burn pits. “From as close as ten feet away,” he said, “I saw nuclear, biological, and medical waste—including bloody cotton gauze, plastics, tires, petroleum cans, oil, and lubricants—thrown into burn pits.” One government investigation found that KBR ignored military regulations designed to protect soldiers; another found that the company systematically hid what it was doing, refusing to share

“proprietary” information on its procedures with the military. Lamberth testified that when he tried to report violations, his supervisors at KBR ordered him to “shut up and keep it to myself.” If he went public, they warned, the company would sue him for slander.

As the burning continued, more and more soldiers got sick. Sergeant Zachary Bell, a marine rifleman who served in Afghanistan from 2007 to 2010, suffers from painful welts all over his arms. Sometimes his hands go numb, or he breaks out in rashes, or he goes into full anaphylactic shock. When he went to Veterans Affairs, the doctors gave him pain pills, sleeping pills—500 mg of Hydrocodone, Valium, and Ambien. All his friends from the war have unexplained illnesses. Everyone suffers from chronic pain. Many have been unable to work. Some of them cough up black stuff. “A few of them have the skin thing, too,” Bell tells me. He sometimes rolls up his sleeves to show people his welts. “It’s a crowd pleaser,” he says.

In most cases, when veterans have sought treatment or disability benefits from the VA for exposure to burn-pit

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Kellogg Brown & Root made millions of dollars operating burn pits in Afghanistan and Iraq. The firm ignored safety regulations and failed to switch to incinerators, even after soldiers began falling ill.

smoke, their claims have been rejected. The Defense Department maintains that there is no proof that the burn pits made soldiers sick. Troops in Iraq and Afghanistan were exposed to a host of environmental hazards: There were toxic particles in dust and sand, chemicals in fuel and exhaust fumes, industrial accidents and sulfur fires. From a purely diagnostic standpoint, ailing veterans could have been injured by any one of these factors, or a combination of them, or none of them at all. By 2010, at least six years after soldiers began falling ill, the Defense Department was still assuring Congress that open-air burning was “the safest, most effective, and most expedient” means to dispose of military trash in a combat theater.

What is happening with the burn pits follows an all-too-familiar pattern of official dishonesty and deception that has been repeated in war after war. First comes denial: The VA didn’t acknowledge the damage caused by Agent Orange until 1991, nearly two decades after combat troops withdrew from Vietnam, and for years it dismissed the neurological condition known as Gulf War syndrome as psychosomatic. Then, once veterans begin to protest, the military agrees to “study the problem.” Next, it stalls for as long as possible: Long-term studies are commissioned—some of which can take decades. And finally, the government manipulates the outcome to reach the desired conclusion: that there isn’t enough data to confirm a correlation between

the illness and its apparent source. Again and again, from Saigon to Kabul, the government has designed inadequate studies, manipulated data, and ignored relevant academic research, all to avoid responsibility for the harm done to our soldiers. Their illnesses linger and worsen. For some ailing veterans, the delay effectively serves as a death sentence.

“It took the government years to recognize that there was a link between Agent Orange and the devastating health effects on our soldiers,” Senator Amy Klobuchar, a Democrat from Minnesota, and Senator Thom Tillis, a Republican from North Carolina, observed in an op-ed for Fox News in May. “Veterans had to wait to get the care they desperately needed and clearly earned. Today we have a new Agent Orange: burn pits.”

Senior Master Sergeant Jessey Baca was in his mid-forties and in good health before he served two tours in Iraq. He liked to run—he did a half-marathon once— and to raise green chilies in his garden in Albuquerque. He’s been married for 38 years and has two children and four grandchildren. On his first tour, in 2004, he spent six months at Balad, as an aircraft maintenance technician for the New Mexico Air National Guard. He worked, ate, and slept near the burn pits. “The smoke was blue and knee-deep, like a fog,” he says. “I had to dust myself off from all the ash falling on me.”

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Soldiers housed near the massive burn pit at Joint Base Balad began coughing up black mucus, which they called “black goop” or “Iraqi crud.”

After his first tour, he began suffering from flulike symptoms and upper respiratory problems. His doctors in Albuquerque told him he had a cold. Baca had fevers that wouldn’t go away, cold chills and night sweats, a persistent cough, and blood in his mucus. The doctors subjected him to a battery of tests, all of which came back inconclusive— “their favorite word,” as Baca puts it.

In 2007 he passed his deployment physical and returned to Iraq, again at Balad. This time, his health got much worse. He spent part of his tour on bed rest. At one point, he noticed a spot on his nose; every time he touched it, it would bleed. After he got home, he suffered from massive headaches, chronic fatigue, and hearing loss. He had trouble breathing. He was diagnosed with basal cell carcinoma, three layers deep into his skin. There were lumps on the side of his face below the jawline. His body hair fell out. His hands swelled and developed lumps, which turned out to be tumors.

At the VA in Albuquerque, the doctors told his wife, Maria, that Jessey had post-traumatic stress disorder. “ptsd doesn’t cause tumors,” she replied. “It doesn’t cause coughing up blood. It doesn’t cause bronchitis.” She was informed that her reaction was part of the problem. “It’s wives like you that cause soldiers to commit suicide,” a VA staffer told her. “Because you won’t admit they have ptsd.”

Baca never denied he had ptsd. “But, you know, I also had tumors,” he says.

Baca went from one VA to the next, one doctor to the next, test after test, hoping for an explanation. He ticks off the list: “MRIs, CT scans, x-rays, vials of blood, and more blood.” He saw pulmonologists and rheumatologists, infection specialists and internists, orthopedists. They could find his sickness—it

was everywhere—but they couldn’t tell him what was causing it. The VA denied that his ailments were service-related, so he was forced to pay for a lot of the treatment out of his own pocket. The VA also denied him disability, so he kept on fixing airplanes, even as it became hard to walk or breathe.

Finally, a doctor at National Jewish Health in Denver referred him to Robert Miller, a pulmonary specialist at Vanderbilt University who had conducted a study on veterans from Iraq and Afghanistan with post-deployment respiratory problems. Like Baca, many of the soldiers had been exposed to the burn pits. When Miller did biopsies on the vets, he

found that a high percentage of them had constrictive bronchiolitis, an incurable and often terminal illness. “It’s an untreatable disease,” Miller said at the time. “We don’t know what’s going to happen to these people down the road.”

In 2009, Jessey and Maria arranged to visit Miller in Nashville. But before they left, they learned that their insurance wouldn’t pay for the visit because it was out of network. Baca went to Vanderbilt anyway. Miller did a lung biopsy. The results were as Baca feared: He had constrictive bronchiolitis. He was going to die.

But he also felt a sense of relief. With a diagnosis, he could finally receive disability benefits. It took three years for his first claim to be granted. By then, he and Maria were exhausted and nearly broke. All told, they had paid more than $200,000 for private insurance. When they needed airfare to visit specialists, they had to ask a group called Angel Airlines for Veterans to pay for the ticket. “We should be able to seek the treatment we needed without begging for help,” Maria says.

Maria didn’t want other veterans to have the same experience, so she looked around online for a place to let them know about Miller’s research. She came across a Facebook page called Burn Pit, where veterans and their families shared stories about doctors and the VA. Maria posted a message about Miller’s research on the page.

“I didn’t expect a response,” she says. “But I was flooded with messages from vets who were fed up with the VA and wanted diagnoses for illnesses they believed were caused by burn-pit exposure.”

To help spur action, Maria decided to start her own Facebook page, Burn Pit Families. Nine veterans and their families replied to Maria, and they began working together. Staff Sergeant Tim Wymore, who served at Balad in 2004, had lost most of his colon to a bacterial infection. He suffered from a host of severe illnesses, including constrictive bronchiolitis, as did Captain Le Roy Torres and Sergeant Aubrey Tapley. Sergeant Bill McKenna had stage four lymphoma. Steven Ochs, an Army paratrooper, and Matthew Bumpus, an Army staff sergeant, had died recently of acute myeloid leukemia, a rare and aggressive form of cancer. Kevin Wilkins, a registered nurse in the Air Force Reserve, had also died of a rare brain cancer after serving at Balad. He was represented by his wife, Jill, who had started the Facebook page Maria used.

In 2009, Baca joined other veterans and military contractors who filed a lawsuit against KBR for negligence and “willful and wanton conduct.” KBR has denied responsibility, insisting that it operated burn pits “safely and effectively.” The company also tried to have the lawsuit dismissed, arguing that it had “derivative sovereign immunity,” which means it couldn’t be sued because it was acting as an extension of the U.S. military. Last year, however, the Supreme Court declined to review the KBR case, which has grown to 800 people, allowing the lawsuit to go forward.

On the legislative front, Jessey and Maria worked with Senator Tom Udall, who drafted a bill calling for the creation of an official registry for burn-pit patients. This was the same pattern that the government had followed when veterans

What is happening with the burn pits follows an all-too- familiar pattern of official dishonesty and deception that has been repeated in war after war.

26 | NEW REPUBLIC

began suffering from mysterious health problems after the Gulf War: beginning the arduous process of assembling a list of those who had been exposed. Jessey and Maria traveled to Washington at their own expense to support Udall’s bill, which Congress passed in 2012.

The registry did not guarantee medical treatment or disability payments to veterans who had been exposed to burn pits. Instead, it was established only to gather information “necessary to ascertain and monitor the health effects of such exposure.” In short, it committed the government to study the problem. After another two years of delays, the registry opened in June 2014. More than 90,000 veterans have registered.

Baca calls the registry “a milestone for veterans” that “brought awareness to the issue, like with Agent Orange.” But in the two years since the registry was created, little has changed. In January, Stars and Stripes reported that the U.S. military was still using a burn pit to dispose of medical waste at the al-Taqaddum Air Base in Iraq—years after the government required the use of incinerators. And in March, Senator Klobuchar introduced a bill that would require the VA to create a national “center for excellence” for the “prevention, diagnosis, mitigation, treatment, and rehabilitation of health conditions relating to exposure to burn pits.” According to GovTrack, an independent

organization that monitors congressional legislation, the bill has a 1 percent chance of being enacted.

On its public health web page, the VA has posted a terse, official statement about burn pits. “At this time,” it reads, “research does not show evidence of long-term health problems from exposure to burn pits.”

This statement is untrue, in the way that official statements are often untrue: not because it contains an outright lie, but because it twists the meaning of everyday words like research and evidence. As the VA knows, there has, in fact, been significant research into burn pits by reputable scientists at established academic institutions, who have published their findings in major, peer-reviewed publications. And that research strongly suggests that long-term health problems among veterans may well have been caused by exposure to burn pits.

One of the first studies was conducted by Miller, the professor of clinical medicine at Vanderbilt. In 2004, soldiers from the 101st Airborne returned from a one-year deployment in Iraq and were stationed at Fort Campbell, not far from the university. Some were so short of breath, they were unable to complete the Army’s two-mile run—one of the military’s most basic tests for physical readiness to deploy. Physical readiness PH

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Jessey Baca, at home in October. Exposed to burn pits, he suffers from a deadly respiratory disease: “It feels like a cactus growing in my lungs.”

is an important factor in determining “service connection,” the causal link for military-related illnesses that obligates the VA to provide medical care or disability benefits.

A soldier who has completed a tour of duty was, by definition, physically fit prior to deployment. So when healthy soldiers are suddenly unable to complete the same test they passed prior to deployment, there is a baseline indication that something happened to them during their service that caused their health to deteriorate. As Miller later recalled, what each soldier told him was remarkably consistent: “I was elite. I was athletic. I was deployed. And now I can’t do my two-mile run, and I’m not deployable.”

Miller’s study was published in 2011 in the New England Journal of Medicine. In a related paper, he observed that constrictive bronchiolitis “rarely occurs in otherwise healthy and athletic individuals. It is known to result from toxic inhalation.” He also noted that researchers at National Jewish Health in Denver found similar patterns of constrictive bronchiolitis among soldiers exposed to burn pits.

Other academic researchers were also studying how burn pits had injured soldiers. In 2004, Anthony Szema, an occupational medicine and epidemiology expert at Hofstra, noticed a sudden shift in the kind of patients who came to him for treatment. “Before, I mostly saw 80-year-old veterans,” he recalls. “Now I saw young women and men, previously healthy soldiers, who were out of breath and suffering respiratory illnesses, including asthma, and no longer fit to deploy.”

When asthma medication didn’t improve their conditions, Szema began conducting a series of tests to figure out what was wrong. He acquired three sets of dust samples: one from sand taken from the San Joaquin Valley in California; another from a titanium mine in Montana; and a third from a burn pit at Camp Victory in Iraq. When Szema pumped the samples into the lungs of laboratory mice, the result was striking: Mice

that inhaled the Camp Victory dust suffered the highest levels of lung inflammation and suppressed t-cells, which form the core of the body’s immune system. The study was published in the Journal of Occupational and Environmental Medicine.

While Szema’s sample size was tiny—only 13 mice—the results matched what he saw among the soldiers he treated. “Humans are not supposed to breathe in particles,” he says. “If we breathe in high concentrations of particulate matter, we

will suffer prematurely, of lung disease or asthma, regardless of where the particles are coming from. Humans should not be inhaling smoke. We should not be burning trash. In Iraq, the trash is fueled by jet fuel. Do you want to breathe jet fuel?”

Szema compares burn-pit exposure to the illnesses suffered by firefighters, police, and other 9/11 workers after the collapse of the World Trade Center. “The exposure is much worse in Iraq,” he says. “Not only were many of these guys deployed for a whole year, but in addition to burn pits, there are tons of other exposure sources. It’s a multifactorial issue. If you’re not dead after the Humvee explodes, then you are going to breathe in bits of the vaporized Humvee. Whatever they aim at you over there, it blows up. Then you head back to base after battle and hang out and breathe in all the smoke from trash fires, because the smoke was in the mess halls and bathrooms and barracks.”

The issue of multifactorial exposure is at the heart of the battle over burn-pit disabilities. Because troops were exposed to so many health hazards, from sandstorms to IED blasts to mine fires, it is extremely difficult—if not impossible— to isolate a single cause behind a rash of ailments with absolute certainty. But for many soldiers, Szema notes, the burn pits delivered a steady stream of toxic chemicals straight into their lungs, day and night. “The lungs are our body’s filters,” he says. “Go to Iraq and your lungs are like the back of an air conditioner you haven’t changed for five years. It’s like Iraq is coming out of their lungs.”

The government’s response to these studies has been emblematic of its past approach to service- related illnesses among veterans. First, it sought to debunk the early research. Then, it manipulated its own studies to ensure that the outcome would arrive at the word so many burn-pit soldiers have come to dread: inconclusive.

In 2009, the VA commissioned a major study of burn pits, focused on the Balad base. The study was conducted by the Health and Medicine Division—previously known as the Institute of Medicine—at the National Academy of Medicine. HMD’s mission is to “provide independent, objective analysis” that will help “solve complex problems and inform public policy decisions related to science, technology, and medicine.” In practice, however, HMD faces the same pressure any other consulting organization faces: to produce results that will please its client. More than half of all funding for HMD and the National Academy of Medicine comes from the federal government, including 13 percent from the VA. The HMD study on burn pits, in short, was underwritten by the very agency potentially facing billions of dollars in insurance claims from veterans exposed to burn pits.

In 2011, after two years of study, HMD issued a report entitled “Long-Term Health Consequences of Exposure to Burn Pits in Iraq and Afghanistan.” The report wasted no time dismissing the “concerns” expressed by ailing veterans. The public furor, it suggested, had been created by “articles in the popular press” and “anecdotal reports.”

“Humans should not be inhaling smoke,” Szema says.

“We should not be burning trash. In Iraq, the trash is fueled by jet fuel. Do you want to breathe jet fuel?”

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Such reports, HMD warned, “do not demonstrate causality or even association; the committee looked instead to the epidemiologic literature on the exposed populations, and on populations similarly exposed.”

HMD’s own conclusion amounted to one big scientific shrug. Its researchers reported that they were “unable to say whether exposures to emissions from the burn pit at Joint Base Balad have caused long-term health effects.” They conceded only that service in Iraq and Afghanistan “might” be associated with long-term health effects. They also recommended further study—not of burn pits, but a “broader consideration of air pollution.”

A closer look at the study, however, reveals that the HMD shaped the methodology and data to avoid linking burn pits to the widespread suffering among veterans. The research protocol it followed required a “risk assessment process” for contamination that was first developed by the Nuclear Regulatory Commission in 1983. The process sounds straightforward enough: First, you study the contamination level of a specific place, such as Balad. Then, you figure out the inherent toxicity of the chemical and how many people were exposed. After that, you review research published

on comparable contaminations—cancer among victims at Chernobyl, say, or residents of Love Canal. The result, in theory, should yield a scientifically rigorous prediction of how likely the contamination was to make people sick.

When it comes to burn pits, however, that kind of risk assessment simply isn’t possible. In its report, HMD concedes that the Defense Department does not possess adequate data on Balad. It doesn’t know what was burned, or how often soldiers worked in the pits, or how many troops lived nearby, or how long they lived there. It doesn’t know the frequency of smoke exposure, or the combination of pollutants involved, or what other contamination soldiers might have been exposed to, either on base or off. The Pentagon was conducting a war, not a science experiment. And as in past wars, it did not pause to assess whether its own practices—something as seemingly mundane as burning trash—might be placing soldiers at serious risk. After Vietnam, the government was unable to say exactly how much Agent Orange soldiers were exposed to. After the Gulf War, it could not account for the combination of toxic elements that contributed to veterans falling ill: depleted uranium, smoke from burning oil wells, vaccinations, sarin gas. The VA, in fact, still refuses to refer to the debilitating condition suffered by Gulf War vets as a “syndrome.” It prefers a more revealing term: “medically unexplained illnesses.” For the military, the health and well-being of veterans is simply another known unknown.

Faced with a lack of accurate data on human exposure in Iraq and Afghanistan, HMD had a clear alternative, one that would meet the prevailing scientific standard for such research: a review of toxicity studies on animals. While such a review would not be comprehensive, it would help determine whether burn pits had made soldiers sick. That, in turn, would allow veterans to know if their ailments were service-related, which would force the VA to provide them with treatment and disability. But instead of following established scientific protocol, HMD made a decision that fatally undercut its findings: It refused to consider animal studies in reaching its conclusions.

HMD researchers had been working for years to skew their studies in favor of the VA. In 1994, when HMD published its first study on the impact of Agent Orange on U.S. soldiers, its own research standards required it to rely on both human and animal studies. That study confirmed a link between Agent Orange, a military herbicide, and widespread health problems among Vietnam vets.

By 1998, though, when HMD began its studies of Gulf War exposures, it had made a subtle but significant change to its standards for “categories of evidence.” Animal studies could still be discussed in its reports, but they were no longer considered valid evidence as part of its final conclusions. The science, in short, was being rigged to reach a desired outcome.

A year earlier, a congressional investigation had called the government’s approach to studying Gulf War illnesses “irreparably flawed.” In response, Congress created the Research Advisory Committee to conduct an independent

DECEMBER 2016 | 29

This is a caption that will go in this space ….

In Anthony Szema’s study, dust samples from Camp Victory (top) injured the immune system in mice. Electron microscopy of the dust (above) found particulates that likely caused lung scarring in veterans.

study. The RAC reviewed evidence from nearly 2,000 scientific studies and government reports, including both human and animal studies. Unlike HMD, which stated that it was not its responsibility “to determine whether a unique Gulf War syndrome exists,” the RAC found that the illness was “real” and that it “affects at least one-fourth of those who served in the war, is not associated with psychiatric illness, and was caused by toxic exposures including pesticides, pyridostigmine bromide pills, and possibly oil well fires, multiple vaccinations, and low-level nerve gas released by the destruction of Iraqi facilities.”

When it came time to study burn pits, however, HMD once again relied on flawed methodology. Lacking human data on Balad, researchers decided instead to look at two nonmilitary populations it defined as similar to soldiers who served at Balad: firefighters, including those exposed to chemical blazes and wildfires, as well as incinerator workers. HMD acknowledged that the experience of firefighters is “likely to differ from the chronic exposures to burn-pit emissions that military personnel experience.” But it still contended that this group was “the best available representation of exposures to mixtures of combustion products.”

It’s not hard to see how HMD’s methodology would corrupt its findings. Firefighters inhale smoke only for brief periods, unlike the around-the-clock exposure experienced by soldiers who lived and worked next to burn pits in Iraq

and Afghanistan. And incinerator workers, by definition, inhale cleaner-burning smoke that has been run through an incinerator—the very same equipment that KBR failed to deploy at Balad and other military bases. Demonstrating a low risk to firefighters and incinerator workers would tell you next to nothing about the connection between burn pits and ailing veterans.

“You have a concern about people coming back, people getting ill, and then do you go do a study by comparing their health to people back home?” says James Binns, who chaired the RAC that studied Gulf War illnesses. “This was a study designed not to detect the problems, but to dilute the problems.”

In an email to the new republic, HMD defended its methodology. It cited the complex mix of chemicals released by the burn pits, and said that it did not know “if the black smoke that everyone complained about had been sampled.” While it would have been “nice,” HMD added, to have reliable studies in which animals were exposed to burn-pit emissions with the same intensity and frequency as soldiers, “these types of studies are difficult, expensive, and time-consuming to conduct.”

The VA employed a similar form of scientific self-dealing in 2009, when it conducted a national survey on the health of more than 20,500 veterans who had been deployed during the wars in Iraq and Afghanistan. Steven Coughlin,

30 | NEW REPUBLIC

Jill Wilkins, the founder of Burn Pit, with her children at Florida National Cemetery in 2010. Jill’s husband, Kevin, was exposed to burn-pit smoke in Balad and died of a brain tumor in 2008. “Kevin was in perfect health before he went to Iraq,” Wilkins says.

a senior epidemiologist at the VA’s Office of Public Health, used data from the survey to study the link between burn- pit exposure and respiratory illnesses such as asthma and bronchitis. Coughlin, who had run the public health ethics program at Tulane University and who co-wrote the ethics guidelines for the American College of Epidemiology, found a positive correlation between soldiers exposed to the burn pits in Iraq and Afghanistan and the onset of chronic ailments. But when he shared his findings with his supervisor at the VA, he was ordered to stop looking into the data for such connections.

“We set the findings aside,” Coughlin says. “Tabled them. Discarded them. They decided not to include the burn-pit exposures, and focus simply on the frequency of respiratory illness. They wanted to ‘simplify’ the analysis. It became clear that they were trying to suppress the findings and downplay the associations instead of highlighting them.”

Coughlin resigned from the VA in 2012. It was untenable, he concluded, to conduct scientific research on behalf of an agency that, like any insurance company, had a direct financial motivation to deny claims to its patients. “There’s a conflict of interest within the VA,” Coughlin says. “As they find new deployment-related health conditions, like the conditions associated with Agent Orange exposure during Vietnam, it ends up costing them billions of dollars.”

In a sense, the wars in Afghanistan and Iraq began with a burn pit. When the Twin Towers collapsed on September 11, the bombing incinerated hundreds of thousands of tons of cement, steel, drywall, window glass, computers, and electrical cables. A toxic plume arose from

the site, and the dust that settled over the city included the remains of the 2,753 people killed in the attack. It was, in more ways than one, a foreshadowing of what was to come.

In the weeks following the attacks, the Environmental Protection Agency assured New Yorkers that the dust and smoke from Ground Zero did not pose a health risk. But by the time the United States invaded Iraq in 2003, it had become clear that those assurances were a lie driven not by science, but by politics: The Bush administration, it turned out, had pressured the EPA to downplay the risk posed by

Ground Zero exposure. As 9/11 first responders began to develop cancer and die, the government fell into the pattern of evasion that continues to this day: deny the problem exists, delay taking action for as long as possible, create a registry of those who complain, order a study, spin the findings, and then order another study.

In June 2015, the VA finally published findings drawn from the burn-pit registry, based on questionnaires completed by 27,000 veterans who said they had been exposed to burn pits. (Nearly all of the vets also reported being exposed to dust storms at some point during their deployment.) Those exposed to burn pits suffered from higher rates of asthma, emphysema, and rare lung disorders. Thirty percent had been diagnosed with respiratory diseases, including serious disorders like chronic obstructive pulmonary disease and chronic bronchitis. Three hundred and sixty five veterans said they had been diagnosed with constrictive bronchiolitis or idiopathic pulmonary fibrosis, another incurable lung disease, typically not found in young, fit populations.

Such numbers almost certainly underestimate the scope and severity of the health crisis among veterans of America’s wars in Iraq and Afghanistan. Many cancers don’t reveal themselves for a decade or more, and many serious respiratory symptoms tend to be misdiagnosed as asthma. When veterans develop respiratory disorders after they return home, doctors may fail to make a connection between their symptoms and their military service. The truth is, we may never have a full scientific understanding of the pain and suffering that the burn pits inflicted on U.S. soldiers. And the VA is taking advantage of that fact to withhold medical treatment and disability benefits from those who were injured overseas. For veterans exposed to the burn pits, the equation is simple: Every delay by the government means less treatment, higher medical costs, and a greater risk of death.

In February 2015, Jessey and Maria Baca traveled to New York City. They had put together a “bucket list” of things Jessey wanted to do before he died, and visiting the city was on it. When I meet them in the lobby of a Holiday Inn on Wall Street, not far from the World Trade Center site, Jessey shows me a red welt on his cheek.

“No idea why,” he says. “Weird new things all the time.” “This is him on a good day,” Maria adds. “It feels like a cactus growing in my lungs,” Jessey says.

“I can breathe in, but not always out.” Maria tells me that another of the veterans who worked

to create the burn-pit registry had died. Bill McKenna didn’t live to see the registry open: He died of a cancerous mass on his heart in 2010. He was 42 years old and had never smoked.

Baca knows he has been treated unfairly. But he is glad that he managed to receive a diagnosis before he dies, and that he forced the government to acknowledge he was injured in service to his country. “I’m one of the lucky ones,” he says.

I ask why he thinks that. “The worst part was the unknown,” he says. “I didn’t want

to die of the unknown.” a

For veterans exposed to the burn pits, every delay by the government means less treatment, higher medical costs, and a greater risk of death.

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President George H. W. Bush’s loss in the 1992 general election was a setback to American agri-culture. no longer did the nation have a White House eager to advance the use of relatively new techniques of molecular genetic engineering—the prototype of which was recombinant DnA technology, or “genetic modification” (GM). instead, during Bill Clinton’s administration, with agricultural biotechnology (and other federal technology policy) under the influence of Vice President Al Gore, the policy direction shifted toward the excessive and unnecessary regulation that he had sought unsuccessfully to impose while in Congress.

A prime example is the U.S. Food and Drug Administration’s 1993 decision to expand its regulatory oversight to include all “genetically modified” animals, including insects. this move was surprising for a couple of reasons.

First, the FDA’s Center for Veterinary Medicine decided to subject genetically engineered animals and insects to the same rig- orous, burdensome pre-market research and approval procedures and regulations as new veterinary drugs such as antibiotics, pain relievers, and anti-flea medicines. the rationale was that the new DnA in the animal and any proteins it expresses are analogous to drugs that have been injected or ingested—even though animals with identical traits introduced by techniques such as natural breeding, artificial insemination, irradiation, or cloning would not be subject to any premarket review at all.

Second, the U.S. Department of Agriculture—not the FDA— had long been the agency most experienced in dealing with farm animals. And both the USDA and ePA had regulated insect

John J. Cohrssen formerly was counsel to the White house Biotechnology Working Group, associate director of the President’s Council on Competitiveness, and counsel for the house energy and Commerce Committee. henry I. MIller, a physician, is the robert Wesson Fellow in scientific Philosophy and Public Policy at stanford University’s hoover Institution. he was the founding director of the office of Biotechnology at the U.s. Food and Drug Administration.

Stunted HarveSt

Regulatory reform for biotechnology is a tough row to hoe. ✒ By John J. Cohrssen AnD henry I. MIller

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biological control agents, which have been used successfully for more than half a century.

FIsh story

the FDA’s long review times have virtually obliterated the once- promising biotechnology sector of new, improved food animals. Under its authority to regulate veterinary drugs, the FDA dith- ered for more than 20 years in reviewing the AquAdvantage genetically engineered, faster-growing salmon. After the appli- cation had successfully fulfilled all FDA requirements, includ- ing an environmental assessment (the result of which was “no significant impact”), the decision was hijacked by the Obama White House, where it languished for three years before finally gaining approval this november.

the poor fish that treaded water in regulatory limbo for more than two decades is simply an Atlantic salmon with an added Chinook salmon growth hormone gene that is turned on all year long instead of only during the warmer months, as in nature. this roughly halves the salmon’s time to maturity. the genetic change confers no detectable difference in the salmon’s appearance, ultimate size, taste, or nutritional value; it just grows faster—a tremendous economic advantage in farming the fish in a closed water system. this will benefit consumers, who will have access to a greater supply and lower prices. the availability of the AquAdvantage salmon will also help to alleviate the pressure on populations of wild Atlantic and Pacific salmon, many species of which are threatened or endangered.

the FDA’s exhaustive (and excessively lengthy) analysis con- cluded that the salmon has no detectable differences and that it

“is as safe as food from conventional Atlantic salmon.” Because the farmed fish will be sterile females and farmed inland in a closed system, they will be unable to affect the gene pool. (even if they were to escape somehow, the fish would not adapt well in the wild because they are accustomed to being fed and coddled by humans.)

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a g r i c u l t u r e

this was neither a complicated nor difficult review. the genetic construction consisted of the addition of a gene from another salmon and a snippet of DnA from another fish, the ocean pout, that keeps the gene turned on continuously. there were no other detectable compositional differences. And the farming of only sterile females in a closed system will prevent the AquAdvantage salmon from replicating the horror of the science-gone-wrong B-movie spoof Attack of the Killer Tomatoes.

this excessively lengthy and uncertain regulation has forced some U.S. animal genetic engineering researchers to take their promising work to other countries such as Brazil and China, which offer a friendlier regulatory regime. that means once- highly-touted genetic modifications of animals—such as chickens and cows that produce less environmentally harmful manure, and pigs with muscles that have a higher ratio of protein to fat—are no longer on the horizon, at least in the United States.

PlAnt ProBleMs

Other foods have fared little better. As part of its voluntary review process for new genetically engineered plant varieties, the FDA has performed excruciatingly lengthy reviews instead of what should be routine, rapid evaluations. recent examples include two and four years, respectively, to evaluate and approve bruise- resistant potatoes and non-browning apples, even though the genetic changes were minimal, well circumscribed, and did not involve the insertion of foreign or uncharacterized genetic mate- rial. enzymatic browning is caused by the apple’s intrinsic chemi- cal reaction to cell injury, such as when the fruit is bitten or sliced, which ruptures the cells and triggers a chemical reaction between the enzyme polyphenol oxidase (PPO) and substances in the apple. A family of four genes controls the majority of PPO production. By down-regulating those genes, scientists were able to turn off more than 90 percent of PPO production, giving rise to the “Arctic Apple,” which does not undergo enzymatic browning. the same enzyme-suppression technology has been used to produce the non-browning, low- acrylamide (a presumptive carcinogen)

“innate” potatoes, which are expected to arrive in fast-food outlets later this year.

Mercifully, those plants survived regu- latory review, but the time spent on their reviews was absurd. Complex new pharma- ceuticals that can be prescribed to millions of patients and have potentially significant side effects often are evaluated for safety and effectiveness and approved in less time. When one of the authors of this article, Henry Miller, was the FDA medical reviewer for Humulin (human insulin), the very first bioengineered drug, it was approved in five months. in contrast to the potato and apple reviews, the review of human insulin raised a number of potentially vexing health and environmental issues. the insulin is synthesized in bacteria—e. coli genetically engineered

to synthesize the human protein—so there were concerns that the bacteria could colonize the human gut and the insulin they pro- duced could cause hypoglycemia in drug company workers. there were also concerns about immunological side effects in patients from bacterial material in the purified, injected insulin. But those concerns were handled satisfactorily in less than half a year. in con- trast to drugs, the vast majority of the FDA’s reviews of genetically engineered foods are far less complex—so why do they take so long?

ProteCtIon FroM DAnGeroUs Pests

Delaying the availability of faster-growing salmon or non-brown- ing apples is hardly the end of the world, but the FDA is also drag- ging its feet on badly needed genetically engineered insect-control products that would prevent disease. A company called Oxitec has designed a live mosquito product to reduce the population of mos- quitoes that carry dengue fever and chikungunya. it was approved in Brazil in 2014 after persuasive evidence of safety and efficacy in testing. But in the United States, the FDA has not yet granted permission even for field testing. After protracted delay, a limited, carefully controlled experimental study by the Florida Keys Mos- quito Control District might finally start in the next few months.

Mosquito control is a major public health concern worldwide, with mosquito-borne diseases killing millions of people annually and causing suffering for many more. it takes only one bite from a disease-carrying mosquito to transmit a debilitating or deadly infection, and mosquitoes breed and multiply with astonishing speed. Given that there are no vaccines or drug treatments for illnesses like dengue fever, chikungunya, and West nile virus, and that treatments for diseases like malaria are difficult to access in many at-risk areas, improved mechanisms for controlling mos- quito populations are desperately needed to save lives.

Oxitec’s approach involves the insertion of a lethal gene into

insect embryos using molecular genetic engineering techniques. the modified mosquitoes can only be raised in a laboratory while kept alive by supplementing their diet with the antibiotic tet- racycline. these modified mosquitoes, which are all male (and therefore don’t bite people), are then released to mate with female mosquitoes in the wild. the males impart the lethal gene to their offspring, which, in the absence of the tetracycline supplement to keep them alive, die before adulthood. Continued releases of the

Once-highly-touted genetic modifications of animals— such as chickens and cows that produce less manure, and pigs that have a higher ratio of protein to fat—are no longer on the horizon, at least in the United States.

Winter 2015–2016 / Regulation / 25

engineered mosquitoes cause precipitous declines in wild mosquito populations and a corresponding drop in the diseases they cause.

the Oxitec insect-control technology has important applica- tions for agriculture as well as public health. Last summer, the company announced successful early studies with a genetically modified diamondback moth that could control this destructive pest, which attacks cruciferous vegetables such as broccoli, cab- bage, cauliflower, Brussels sprouts, and radishes.

Given the impaired evolutionary fitness of the Oxitec mos- quitoes, the FDA’s long delays in approving limited field trials are inexplicable. the reason that governments, industries, and academic sponsors perform field trials is to determine safety and efficacy, yet FDA regulators continue to stand in the way of obtaining these essential data.

in contrast to the interminable reviews by the FDA Center for Veterinary Medicine of the faster-maturing salmon and the Oxitec insect-control technology, those same FDA regulators have chosen to exercise “regulatory discretion” to forgo any review at all of the huge numbers of genetically engineered animals used extensively in biomedical research. they also exempted from regulation the widely available GloFish, a genetically engineered fluorescent zebra danio fish for aquariums.

revIsInG the FrAMeWork

the Obama administration recently announced an ambitious White House initiative to update the 30-year-old Coordinated Framework for the regulation of Biotechnology. (Disclosure: the coauthor of this article, John Cohrssen, was legal counsel to the White House working group that developed and implemented the 1986 Coordinated Framework.) the White House has directed the three regulatory agencies with biotechnology oversight—the ePA, FDA, and USDA—to update the Framework and develop a long-term strategy to ensure that the regulatory system is prepared for the future products of biotechnology, using a newly commis- sioned expert analysis of the biotechnology landscape.

By creating an environment that is friendly to biotechnology and the commercialization of products, the Obama White House has a unique opportunity to reduce the regulatory obstacles to continued U.S. advances in agriculture. thirty years of experi- ence with the molecular techniques and products of genetic engineering have proven their versatility, shown that new vari- eties of plants, animals, and microorganisms genetically engi-

neered with molecular techniques have not posed any incremental risks compared to other techniques for genetic modification, and found that once-hypothesized risks have not materialized. Clearly, reforms are needed to make regulation scientifically defensible and risk-based, and to ensure that it provides acceptable cost-benefit.

the White House should adhere to the fundamental principles of the 1986 Coor-

dinated Framework, which remain valid today for the oversight of research and development:

■■ new laws specifically for biotechnology are unnecessary and should be avoided. Biotechnology products can be regulated effectively under the mosaic of existing product-specific laws.

■■ Biotechnology regulation should avoid using a process- based scope, which by definition subjects all products within a defined process-based category to regulation, regardless of whether they are of high, moderate, low, or trivial risk. Such over-regulation not only retards innovation, but also feeds the self-perpetuating, incorrect perception that these prod- ucts must pose a high risk because they are highly regulated.

■■ the degree (intrusiveness) of regulation should be commen- surate with the risk of the product.

What sorts of regulatory changes are needed? the United States should return to the basic tenets of regulation prescribed more than two decades ago in the 1992 White House “scope” docu- ment, which supplemented the 1986 Coordinated Framework:

■■ the scope of regulation should be based on the risk-related characteristics of new products, not on the particular tech- nology that enabled them.

■■ the scope of regulation should be based on evidence that the risk of a particular use of an organism for a particular application is unreasonable.

■■ A genetically engineered organism with new traits posing no greater risk than the unmodified organism should be subject to no greater scope of regulation.

As a practical matter, this means that to the extent appropri- ate, products of biotechnology should be regulated no more stringently than products developed by older and less precise manufacturing processes.

twenty years of continuing White House and regulatory agen- cies’ disregard of the Coordinated Framework and “scope” policies have led to the unnecessary, anti-competitive obstacles to U.S. agricultural applications of biotechnology that the Obama White House now supposedly seeks to address. in order to rationalize regulation, we need to return to a scope of regulation that is based on scientific evidence of an unreasonable risk—the overarching principle adopted by the White House to prevent unnecessary regulatory burdens in the first place.

By creating an environment that is friendly to biotech- nology and the commercialization of products, the Obama White House has an opportunity to reduce the regulatory obstacles to continued U.S. advances in agriculture.

Copyright of Regulation is the property of Cato Institute and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder’s express written permission. However, users may print, download, or email articles for individual use.

Risk Analysis, Vol. 29, No. 12, 2009 DOI: 10.1111/j.1539-6924.2009.01311.x

The Use of Multizone Models to Estimate an Airborne Chemical Contaminant Generation and Decay Profile: Occupational Exposures of Hairdressers to Vinyl Chloride in Hairspray During the 1960s and 1970s

Jennifer Sahmel,1,∗ Ken Unice,2 Paul Scott,2 Dallas Cowan,1 and Dennis Paustenbach3

Vinyl chloride (VC) was used as a propellant in a limited percentage of aerosol hairspray products in the United States from approximately 1967 to 1973. The question has arisen whether occupational exposures of hairdressers to VC-containing hairsprays in hair salons were sufficient to increase the risk for developing hepatic angiosarcoma (HAS). Transient two-zone and steady-state three-zone models were used to estimate the historical airborne concentration of VC for individual hairdressers using hairspray as well as estimated contri- butions from other hairdressers in the same salon. Concentrations of VC were modeled for small, medium, and large salons, as well as a representative home salon. Model inputs were determined using published literature, and variability in these inputs was also considered using Monte Carlo techniques. The 95th percentile for the daily time-weighted average expo- sure for small, medium, and large salons, assuming a market-share fraction of VC-containing hairspray use from the Monte Carlo analysis, was about 0.3 ppm, and for the home salon scenario was 0.1 ppm. The 95th percentile value for the cumulative lifetime exposure of the hairdressers was 2.8 ppm-years for the home salon scenario and 2.0 ppm-years for the small, medium, and large salon scenarios. If using the assumption that all hairsprays used in a salon contained VC, the 95th percentile of the theoretical lifetime cumulative dose was estimated to be 52–79 ppm-years. Estimated lifetime doses were all below the threshold dose for HAS of about 300 to 500 ppm-years reported in the published epidemiology literature.

KEY WORDS: Airborne contaminants; exposure modeling; hairdresser; three-zone model; two-zone model; vinyl chloride

1. INTRODUCTION

Vinyl chloride (VC) is a colorless chlorinated hydrocarbon compound with a sweet odor that ex- ists as a gas at room temperature. The primary use of VC is as a precursor to the chemical intermedi-

1ChemRisk, LLC, Boulder, CO, USA. 2ChemRisk, LLC, Pittsburgh, PA, USA. 3ChemRisk, LLC, San Francisco, CA, USA. ∗Address correspondence to Jennifer Sahmel, Supervising Health

Scientist, 4940 Pearl East Circle, Boulder, CO 80301, USA; tel: 303-417-1046; fax: 303-417-1066; [email protected].

ate polyvinyl chloride (PVC), a component of plas- tic pipes, wall coverings, wire coatings, and vehicle parts. Due to its chemical properties and apparent low toxicity, VC was also used during the 1960s and early 1970s as a propellant in aerosol insecticides, spray paints, and other consumer products. Nonpro- pellant uses including as a refrigerant and inhalable anesthetic have also been documented until its use in consumer products was banned in 1974.(1−3) VC alone has no current consumer applications; it is a confirmed human carcinogen and a highly regulated chemical.

1699 0272-4332/09/0100-1699$22.00/1 C© 2009 Society for Risk Analysis

1700 Sahmel et al.

1.1. VC Toxicity

In the early 1960s, the American Conference of Governmental Industrial Hygienists’ (ACGIH) Threshold Limit Value (TLV) for VC was 500 ppm; Patty’s Industrial Hygiene and Toxicology reported that VC was of relatively low toxicity.(4−6) The tox- icity of VC was established in the early 1970s from case studies of the PVC manufacturing sector, which experienced the highest documented exposures to this compound. Routine maintenance work during PVC production resulted in airborne VC concentra- tions up to 1,000 ppm during the tasks of tank clean- ing and the manual removal of partially polymer- ized PVC from vessel walls with spatulas. These high levels of exposure are believed to have produced a specific pathological syndrome called “vinyl chloride disease.”(7) Symptoms included CNS depression re- sembling alcohol intoxication, headache, dizziness, and acroosteolysis (bone loss and ulceration in the extremities), as well as damage to the liver, spleen, cardiovascular, respiratory, and circulatory sys- tems.(8) In 1971, the first long-term animal study appeared, which reported a possible link between VC exposure and carcinogenic activity, including the possibility of increased incidence of skin, respira- tory, and bone tumors. However, concerns about the methods used in the study resulted in addi- tional toxicological and epidemiological studies on VC.(9) VC was initially linked to a rare form of liver cancer known as hepatic angiosarcoma (HAS) in PVC manufacturing workers through published stud- ies in 1974.(10,11) Subsequent studies have confirmed the link between VC exposures and HAS.(12,13)

HAS has been linked to four different risk fac- tors, including exposures to VC, inorganic arsenic, androgenic anabolic steroids, and thorium dioxide (Thorotrast). For nearly 75% of angiosarcoma cases, however, the cause is unknown.(12) A physiologi- cally based pharmacokinetic (PBPK) model devel- oped to predict cancer risk from VC exposure found that cancer incidence predicted using animal models overestimated the incidence in humans.(14)

1.2. VC Epidemiology and Occupational Exposure Limits

HAS is a rare form of liver cancer even among high-risk populations.(15) During the late 1970s and early 1980s, estimates of HAS incidence within the general population ranged from 0.4 to 2.5 per 10,000,000 in the United States and Europe.(12,16−18)

The range of cumulative VC exposures necessary to increase the risk of disease has also been determined from epidemiology studies. The largest published study to date of PVC workers with documented oc- cupational exposures to VC found no increase in rel- ative risk for HAS below 500 ppm-years of cumula- tive exposure to VC, and also found that the lowest cumulative lifetime exposure to VC for which a doc- umented HAS case occurred was 288 ppm-years.(18)

The latency period associated with VC-related HAS is estimated to be approximately 21 years, with no case identified before 15 years following the first exposure.(18,19)

Following the early epidemiological studies men- tioned above as well as investigations by the Na- tional Institute for Occupational Safety and Health (NIOSH) and the U.S. Congress, the U.S. Occupa- tional Safety and Health Administration (OSHA) reduced the VC permissible exposure limit (PEL) from 100 ppm (parts per million) to 1 ppm in 1974. At the same time, the U.S. Consumer Prod- uct Safety Commission (CPSC) banned the use of VC in consumer products in the United States. Cur- rent occupational exposure limits (OELs) for VC set by both OSHA and ACGIH remain at 1 ppm. Fig. 1 illustrates historical occupational exposure limits established by ACGIH and OSHA for VC

Fig. 1. Occupational exposure limits for VC over time: ACGIH TLV and OSHA PEL. Solid and dotted lines indicate contempo- raneous exposure guidelines as established by the American Con- ference of Governmental Industrial Hygienists (dotted line) and the Occupational Safety and Health Administration (solid line). Guidelines are expressed in parts per million (ppm).

Multizone Exposure Modeling: Historical Use of Vinyl Chloride in Hairspray 1701

beginning in 1946. The VC ban in consumer prod- ucts has remained in place, and the rates of HAS in the general population remain exceedingly low. Among VC workers and other high-risk subgroups, Zocchetti estimated that an increased incidence of HAS of 1,000 times that found in the general popula- tion would only produce one to two cases per year in 10,000 individuals.(15)

In the late 1960s and early 1970s, when VC was used as a propellant in a variety of consumer prod- ucts, many individuals could have been exposed to varying concentrations of VC from either occupa- tional or consumer uses. In particular, the use of VC in occupational settings by hairdressers or hair stylists presents a scenario for which frequent ex- posures might have occurred over time. However, an excess incidence of HAS or other liver cancers has not been found in epidemiological studies of hairdressers.(20−24)

1.3. Hairspray Product Use in the United States During the Time Period of Interest

According to a 1972 U.S. consumer industry analysis, approximately one-half of all American women used hairspray in the early 1970s. Sales of hairsprays grew at about 5.1% per year from 1967 to 1972, a much lower annual increase compared with the first half of the 1960s, and was associated with the rising increase in popularity of more relaxed and nat- ural hairstyles in the late 1960s.(25,26)

Hairsprays in the early 1970s typically consisted of a resin that was capable of forming a thin film on the hair surface (1.5–2% by weight of the for- mulation), ethyl alcohol (42–58% by weight of the formulation), and propellants (30–50% by weight of the formulation). Certain hairsprays also contained additives such as plasticizers, conditioners, and pro- teins. U.S. consumer data in 1972 indicated that there were approximately 150 different brands of hairspray in the market. Sales were highest for the Aqua Net, Breck, and Alberto VO5 brands. Sales of hairsprays to beauty parlors were estimated at about $35 million at the manufacturing level in 1972. Leading brands included La Maur, Alberto-Culver, and Fabergé.(26)

The purpose of our study was two-fold: first, we wanted to present a multizone modeling approach that could provide robust estimates of both expo- sure and risk that could be used in a wide variety of consumer product risk assessments. Second, we wanted to address a concern among the population of hairdressers who believe they could be at increased

risk for HAS as a result of using VC-containing hairsprays prior to 1974. We were unable to find any published studies that measured VC-containing hairspray use among hairdressers. As a result, we used several modeling approaches with multiple con- centration zones (based on contaminant generation source, generation rate, and ventilation characteris- tics, among other factors) to characterize airborne concentrations of VC in salons. The study focuses on VC in aerosol hairspray products for hairdressers in the United States prior to the CPSC ban on the sale of VC-containing consumer products in 1974. In order to characterize possible differences in ex- posure potential and risk related to salon size, sev- eral possible salon sizes were evaluated. Specifically, four scenarios were considered, including a home sa- lon with a single stylist, a small professional salon with an average of two stylists, a medium-sized pro- fessional salon with an average of four stylists, and a large professional salon with an average of nine stylists. A Monte Carlo uncertainty and sensitivity analysis was also conducted. The estimated airborne concentrations and associated cumulative dose esti- mates were then compared against hairspray propel- lant measurement studies and epidemiology studies in the published literature.

2. METHODOLOGY

In order to more accurately estimate the air- borne concentrations in a salon in which a hair- dresser might work, as well as the background con- centrations of VC due to the use of hairspray by other hairdressers, a multizone approach was used to incorporate both types of exposures. First, a two- zone transient model was used for the assessment of hairdresser exposures in a commercial salon en- vironment. Second, both the transient two-zone and a steady-state three-zone model were used to assess hairdresser exposures in a residential environment. Finally, a steady-state mixing factor model was used to confirm and compare against the results of the primary transient two-zone model, mainly to ensure that the results were not dependent upon the model selected.

Estimates of airborne concentration were gener- ated for two types of VC-containing hairspray usage conditions: first, exposure estimates were calculated based on the estimated percentage of hairsprays con- taining VC. This was based on the market availability of these hairsprays. Second, exposure estimates were also calculated for a hypothetical situation in which

1702 Sahmel et al.

all of the hairsprays used in a salon contained VC. Three types of exposure estimates were computed: (a) 15-minute peak concentrations for the period im- mediately after applying hairspray, (b) 8-hour time- weighted averages (TWAs) over a typical salon work day, and (c) working-life VC exposures over the pe- riod in which VC was reported in U.S. hairspray (for the purposes of comparison to occupational exposure limits or risk criteria).

Once point estimates were calculated based on the most likely parameter for each of the four sa- lon scenarios using either the two-zone (commercial and residential salons) or three-zone (residential sa- lon only) model, a Monte Carlo uncertainty and sen- sitivity analysis was conducted. These were intended to characterize the range of possible results based on the parameter uncertainty, and to understand the magnitude of the effect of each of the different pa- rameters on the final model results (i.e., parameter sensitivity). This type of analysis is extremely use- ful for evaluating the uncertainty, for example, lack of precision, in the point estimates for total cumula- tive VC exposure. It also enables one to understand the impact of the unknown precision of certain indi- vidual model parameters. A 95th percentile value for the airborne concentration for each scenario was also calculated using this method to characterize the pos- sible exposure of a worker at the upper end of the distribution.

Following the estimation of exposure concentra- tions using the multizone approach, cumulative ex- posure estimates were calculated for each of the four salon scenarios. Cumulative exposure estimates were calculated assuming a potential exposure time of 8 hours per day, 5 days per week, and 50 weeks per year, and were reported in units of ppm-years. This dose metric allowed for comparison to the epi- demiological literature on VC. Finally, the calculated concentrations were compared to measured data col- lected by Hoffman, which assessed concentrations of hairspray propellants in a working salon prior to 1974.(27)

2.1. The Transient Two-Zone Model

Nicas presented a two-zone model for the pre- diction of both time-variable near-field (NF) breath- ing zone and far-field (FF) room airborne particulate or chemical concentrations in occupational exposure situations.(28) This model was modified to incorpo- rate hairspray usage patterns and generation rates. Model symbols and abbreviations are provided in

Appendix A and a complete list of equations is pro- vided in Appendix B. Briefly, the near field and far field were defined by a pair of coupled mass balance equations:

VN × dCN = [change in mass in NF zone] = (GE/CF1) × dt

+β × CF dt − β × CN × dt = [mass generated inside NF zone]

+ [mass entering NF from FF zone] − [mass leaving NF zone] (1)

VF × dCF = [change in mass in FF zone] = β × CN × dt − [β + Q] × CF × dt = [mass entering from NF zone]

−{[mass leaving FF and entering NF zone] + [mass leaving FF zone and exhausted outside]}

(2)

where VN and VF represented the volumes of the NF and FF zones (m3), CN and CF were the NF and FF airborne concentrations (ppm), GE was the constant mass emission rate (mg/min), β was the airflow rate between the NF and FF zones (m3/min), Q the effec- tive room supply air rate (m3/min), CF1 was a conver- sion factor (mg/m3 per ppm at standard temperature and pressure), and dt was an infinitesimal time inter- val (min) (Appendix A). Each zone in the model was assumed to be well mixed with airflow between the zones (β) dictated by the magnitude of random air- flow (i.e., dispersion) or induced air movements (i.e., fans or blowers) in the space of interest. To construct a daily exposure history, the concentration profiles for multiple hairspray events were superimposed and two sets of solutions to Equations (1) and (2) were used to account for both times during spraying (GE > 0) and after spraying (GE = 0) (Appendix B). The worker’s airborne breathing zone concentration con- sisted of the summation of a worker’s own hairspray usage plus the background contribution of hairspray from co-worker usage.

Ventilation in the FF was defined by the effec- tive room supply air rate (Q) and was comparable to studies of minimum ventilation requirements and the American Society for Heating, Refrigerating, and Air Conditioning Engineers (ASHRAE) room ven- tilation recommendations typically presented in units of cubic feet per minute (cfm). Considering the align- ment of a hairdresser and the aerosol hairspray can,

Multizone Exposure Modeling: Historical Use of Vinyl Chloride in Hairspray 1703

Fig. 2. Conceptual schematic of the two-zone model as applied to a hairspraying scenario. Air exchange in the near field is repre- sented by β while far-field air exchange is represented by Q. The near field is approximated by a hemisphere with the vertical axis in line with the hairdresser’s body while standing behind a customer.

the NF was defined as a hemisphere sliced on the ver- tical axis with the base in line with the hairdresser’s body. A hemisphere radius (RN) of approximately arm’s length or 0.78 m (2.5 ft) was selected for the hairspray scenarios, consistent with the conventional industrial hygiene definition of the breathing zone (Fig. 2)(29) as well as other published studies that have used the transient two-zone model. The two- zone model has been used to predict chemical or par- ticulate exposure for a diverse range of published ex- posure scenarios (Table I).

Equations (1) and (2) do not account for the frac- tion of products that contained VC. Historical doc- umentation indicated that the majority of products between 1967 and 1974 did not contain VC (see de- tailed discussion below); therefore, cumulative expo- sure (ppm-year) model outputs were subsequently adjusted to account for the estimated fraction of products containing VC (FC).

The sensitivity analysis conducted for the results of the transient two-zone model relied upon Monte Carlo statistical techniques to estimate the plausi- ble range of exposures to VC that a stylist might have experienced. The 95th percentile exposure es- timate for each scenario was used to characterize the likely high-end exposure of a worker at the upper end of the exposure distribution. A high-end exposure estimate is defined as conceptually greater than the 90th percentile of the population distribution but not beyond the true maximum exposure.(30) A software

package from Decisioneering Inc. (Boulder, CO) was used to perform this analysis.

2.2. The Three-Zone Steady-State Model

For the home salon scenario, in addition to the transient two-zone model, a three-zone steady-state model consisting of the breathing zone (zone 1), room of use (i.e., home salon, zone 2), and rest of home (zone 3) was used to investigate whether the predicted breathing zone concentration was ap- preciably underestimated by combining together the volume of the room of use and rest of home in the two-zone model.(31) A system of equations represent- ing the mass balance for the three zones was used to calculate the steady-state concentration in each zone (Appendix B). In this model, natural airflow between zones was assumed with balanced flow (i.e., flow from the rest of the home to the salon exactly balanced by flow from the rest of home to the salon). Whole house air exchange was allocated to the salon and rest of home based on the fractional volume of each zone.

2.3. The Steady-State Mixing Factor Model

Although the multizone models were selected as the primary models for this analysis, the steady- state mixing factor model was used for comparison to examine the reproducibility of the model estimates. The multizone models were used because the tran- sient “personal exposure cloud,” which is thought to occur while using hairspray, cannot be easily rep- resented by a conventional steady-state model that pairs the assumptions of a well-mixed room with a safety factor to account for imperfect mixing. However, the steady-state mixing factor model is a frequently used approach described in a number of industrial hygiene texts including the OSHA Techni- cal Manual, ACGIH Manual of Recommended Prac- tice for Design, and AIHA Mathematical Models for Estimating Occupational Exposures to Chemi- cals.(28,32,33) Although the mixing factor approach has been criticized for defying the law of conservation of mass, reasonable agreement between the two-zone model and the steady-state model is achievable with the careful and appropriate selection of mixing fac- tors.(28,34) The steady-state model was included in this assessment to evaluate whether the study con- clusions were affected by model selection.

Gaffney et al. (2008) presented a methodology for relating the steady-state mixing factor model

1704 Sahmel et al.

Table I. Comparison of Application of Two-Zone Model for Commercial Beauty Salons to Other Applications Reported in Peer-Reviewed Literature (29,34,79−90,92,93)

Study Author (Country) Year Scenario Chemical(s)

Near-Field Geometry (Volume)

Flow Rate Between Near Field and

Far-Field Far-Field Air

Change Rate

Sahmel (model shown in Figure 2)

2008 Occupational use of hairspray

Vinyl chloride Hemisphere around breathing zone of radius arm’s length, or 0.78 m [2.5 feet] (1 m3)

5.7 m3/min to 23 m3/min based on random air speed of 0.05–0.20 m/sec

Small salon: 1.3–3.2 Medium salon: 1.3–4.5 Large salon: 3.0–6.9

Gaffney (United States)

2008 Cleaning semiconductor wafers

Methanol Hemisphere above table of radius 1 m (2.1 m3)

11.3 m3/min 5.1–9.5 per hour

Armstrong (United States)

2007 Quantitative microbial risk assessment (QMRA) model for Legionnaires’ disease at whirlpool spa

Legionella Cylinder around spa (>38 m3)

>90 m3/min based on geometric mean random air speed of 0.06 m/s and minimum cylinder radius of 2 m

0.5–1.2 per hour based on mixing height of 3 m

Eickmann (Germany)

2007 Generic two-zone model description

Not applicable Hemisphere, sphere, or cube

Not applicable Not applicable

Spencer (United States)

2007 Solvent exposure during metal part disassembly

Solvent (e.g., cyclohexane)

Hemisphere around work zone of radius 1 m with no flow across flat face (2.1 m3)

10.34 m3/min [enclosed area with no ventilation] to 190 m3/min [well-ventilated] based on random air speed of 0.06 to 1 m/sec

4.3 per hour

Keil (United States) 2006 Chemical exposure at a university teaching laboratory

Methylene chloride Hemisphere around work zone of radius 1 m (2.1 m3)

Average of 11.2 m3/min based on random air speed of 0.06 m/sec

17–20 per hour

Nicas (United States)

2006 Solvent parts washer usage

Benzene Cube around parts washer (0.26 m3)

7.05–11.6 m3/min based on random air speed of 0.15 m/sec

2–3 per hour

Vernez (Switzerland)

2006 Application of waterproofing sprays

Respirable aerosol particles containing solvent

Hemisphere around work zone

8.4–15.65 m3/min 1–3 per hour

Von Grote (Switzerland)

2006 Occupational dry cleaning exposure

Perchloroethylene (PCE)

Cube around dry cleaning stations (100 m3)

13 m3/min to 20 m3/min

6–10 per hour

Vernez (Switzerland)

2004 Application of waterproofing sprays

Respirable aerosol particles containing solvent

Hemisphere around work zone (2 m3)

0.3–1.7 m3/min 1–5 per hour

Keil (United States) 2003 Organic solvent spill

n-pentane Hemisphere around spill with radius 0.5 m (0.26 m3)

2.7 m3/min based on random air speed of 0.57 m/sec

4.9 per hour

Nicas (United States)

2003a Fumigation of commodities– manual processing (e.g., foods)

Methyl bromide Cube at work station (1 m3)

7.7 m3/min [low random air speed condition of 0.05 m/sec]

3 per hour

(Continued)

Multizone Exposure Modeling: Historical Use of Vinyl Chloride in Hairspray 1705

Table I. Continued

Study Author (Country) Year Scenario Chemical(s)

Near-Field Geometry (Volume)

Flow Rate Between Near Field and

Far-Field Far-Field Air

Change Rate

Nicas (United States)

2003b Splash loading of gasoline

Benzene Hemisphere around loading zone with radius 0.76 m (0.92 m3)

13.9 m3/min based on random air speed of 0.13 m/sec

Not specified

Von Grote (Switzerland)

2003 Occupational metal degreasing

Trichloroethylene (TCE) Perchloroethyene (PCE)

Box including degreasing machine and workspace (100 m3)

10–12.5 m3/min 5.5–6.5 per hour

Keil (United States) 2000 Worker located 1 meter from evaporating pollutant in a generic work room

Generic solvent Hemisphere around work zone

5.8–22.1 m3/min based on random air speed of 0.06 m/sec and geometric standard deviation of 0.032

2.4 per hour

Nicas (in Keil 2000, United States)

2000 Application of adhesive

Toluene Hemisphere above table of radius 0.78 m (1 m3)

5 m3/min based on random air speed of 0.04 m/sec

6 per hour

Keil (United States) 1998 Parts washing operation

Toluene Wash station work area

6.7 m3/min Unspecified (room airflow was 766 m3/min)

daily average concentration to the two-zone model represented by the following equations modified to adopt the symbols and units used in this assessment (Appendix B):

CTWA,N =

( GW,day

k + GCW,day

) Q · TW · CF1 (3)

CTWA,F = (GW,day + GCW,day)Q · TW · CF1 (4)

where CTWA,N was the breathing zone concentration (ppm), GW was the constant mass emission rate for the worker of interest (mg/day), GCW was the con- stant mass emission rate for co-worker(s) (mg/day), k was the imperfect mixing factor, Q was the room sup- ply air rate (m3/min), TW was the length of workshift (min/day), and CF1 was a conversion factor (mg/m3

per ppm at standard temperature and pressure).(34)

The imperfect mixing factor was selected based on an analysis of NF to FF concentrations as a function of Q, Vf , and β described by Cherrie et al.(35) For scenarios where the ventilation rate is very low, the steady-state model tends to overestimate true expo- sure if the concentration profile has not returned to

background levels at the end of the exposure period. Therefore, the steady-state approach provides a con- servative or higher estimate of exposure.

2.4. Selection of Model Parameters

A detailed literature search was conducted for each model parameter where possible or applicable to ensure that each was fully characterized for the particular scenarios of interest. A description of each key parameter is provided below and summarized in Table II. The ranges and probability distributions used in the Monte Carlo sensitivity analysis are sum- marized in Table III.

2.4.1. U.S. Fraction of Aerosol Hairspray Products Containing VC (FC)

According to the CPSC’s Bureau of Economic Analysis report entitled Background Analysis of Vinyl Chloride Usage, approximately 2 billion cans of VC-containing aerosol consumer products were filled between 1969 and 1974, which accounted for 15% of the U.S. aerosol production during these years.(36)

Therefore, the total number of cans produced dur- ing this time period was approximately equal to 13.3 billion. The report further estimated that aerosol

1706 Sahmel et al.

Table II. Input Values for the Near-Field/Far-Field Hairspray Propellant Exposure Model

Simulation #1 Simulation #2 Simulation #3 Simulation #4 Residential Setting Small Salon Medium Salon Large Salon

Input Parameters Number of stylists, 1+NCW 1 2 4 9 Maximum number of occupants, NO 3 6 12 27

Daily averaging time, TW (minutes) 1440 480 480 480

Years worked during VC usage, DH 7.25 7.25 7.25 7.25

Occupational equivalent years worked during VC usage, OEa

21.75 7.25 7.25 7.25

Radius of near-field hemisphere, RN (m)

0.78 0.78 0.78 0.78

Far-field volume (commercial salon or total residential volume), VF (m3)b

356 142 198 275

Random air speed, S (m/min) 6.0 6.0 6.0 6.0

Unit ventilation rate, Q’ (m3/min/person)c,d

– 0.708 0.708 0.708

Residential air exchange rate, AR (hr−1)c

0.87 – – –

Spray frequency—worker, EW (events/day)e

9.5 9.5 9.5 9.5

Spray frequency—co-worker(s), ECW (events/day)e

0 9.5 28.5 76

Mass of hairspray applied per customer, ME (g/customer)

12 12 12 12

Hairspray generation rate, GH (g/min)

34.2 34.2 34.2 34.2

Average VC content, WH (%/w/w)f 10% 10% 10% 10%

Percentage of aerosol hairspray cans containing VC, FC (%)

3.50% 3.50% 3.50% 3.50%

Imperfect mixing factor—steady-state model, k (hr−1)

0.6 0.7 0.5 0.4

Conversion factor, CF1 (mg/m3 per ppm at standard conditions)

2.56 2.56 2.56 2.56

Calculated Parametersg

Near-field volume, VN (m3) 0.994 0.994 0.994 0.994

Interzonal airflow, β(m3/min) 11.47 11.47 11.47 11.47

Salon or residence air flow, Q (m3/min)c

5.162 4.248 8.496 19.116

VC generation rate GE (mg/min) 3420 3420 3420 3420

Commercial air exchange rate, AC (hr−1)

– 1.8 2.6 4.2

Spray duration, TE (min) 0.35 0.35 0.35 0.35

aStandard occupational year defined as 5 days/week, 50 weeks/year, and 8 hours/day equal to 2,000 hours/year. Residential setting includes a total of 24 hours consisting of 8 hours working and 16 hours in the home after working for a total of 6,000 hours per year. bA home size of 356 m3 was selected based on 1980 data from the U.S. Department of Energy on single-family home floor area distribution with an assumption of 2.4 m ceilings. cResidential ventilation rate based on air exchange rate data; commercial ventilation rate based on contemporaneous rules and practices. dFlow rate of 0.708 m3/min/person equates to 25 cfm/person. eExpected value based on Pr[E] and Pr[Ej = k | n] as described in Appendix B. fBased on the weighted average midpoint content by year for products sold on the market of 12.5% for 1967 to 1968, 8.9% (range = 5.2–12.5%). gSee Appendix B for equations used to determine calculated parameters.

Multizone Exposure Modeling: Historical Use of Vinyl Chloride in Hairspray 1707

Table III. Probability Distributions Assigned for the Near-Field/Far-Field Model and Predicted Cumulative Exposure Based on 10,000 Monte Carlo Iterations

Probability Distributions Assigneda

Simulation #1 Simulation #2 Simulation #3 Simulation #4 Residential Setting Small Salon Medium Salon Large Salon

Model Input Random air speed, S (m/min) Triangular Triangular Triangular Triangular

[3, 12] [3, 12] [3, 12] [3, 12] Mode = 6 Mode = 6 Mode = 6 Mode = 6

Unit commercial ventilation rate, Q’ Triangular Triangular Triangular (m3/min/person)b Not applicable [0.425, 0.991] [0.425, 0.991] [0.425, 0.991]

Mode = 0.708 Mode = 0.708 Mode = 0.708 Residential air exchange rate, AR (hr−1) Lognormal

Geo. mean = 0.68 Not applicable Not applicable Not applicable Geo. std. dev. = 2.01

Probability of a customer per 15-minute period (per stylist), Pr[E]c

29.6% 29.6% 29.6% 29.6%

Shop or home volume, VF (m3) Empirical 113 to 226 (21.2%) Triangular Triangular Triangular 226 to 340 (33.3%) [59, 192] [69, 411] [137, 357] 340 to 453 (22.7%) Mode = 142 Mode = 198 Mode = 275 453 to 679 (16.7%)

679 (6.1%)

Mass of hairspray applied per customer, ME Triangular Triangular Triangular Triangular (g/customer) [6.3, 16.3] [6.3, 16.3] [6.3, 16.3] [6.3, 16.3]

Mode = 12 Mode = 12 Mode = 12 Mode = 12 Hairspray Generation Rate, GH (g/min)d Triangular Triangular Triangular Triangular

[18, 46] [18, 46] [18, 46] [18, 46] Mode = 34 Mode = 34 Mode = 34 Mode = 34

VC content, WH (%/w/w) 1967–1968:12.5% 1969 uniform [6%, 12.5%]

1970–1972: uniform [5.2%, 12.5%] 1973–1974: uniform [6%, 12.5%]

Percentage of aerosol hairspray cans containing Uniform Uniform Uniform Uniform VC, FC (%) [0.4, 6.56] [0.4, 6.56] [0.4, 6.56] [0.4, 6.56]

Model Output Distribution—Cumulative Exposure, CE (ppm-year)

Mean 1.0 1.2 1.2 1.2

CV 0.95 0.38 0.35 0.33

5th percentile 0.23 0.57 0.61 0.66

95th percentile 2.78 2.01 1.95 1.96

aInputs include type of distribution, range, and parameters. bCorresponds to a range of 15–35 cfm/person. cCorresponds to an expected number of customers of 9.5 per day per stylist. dDistribution based on U.S. Department of Energy data for 1980.

cans of paints, finishes, and similar coatings ac- counted for 75–90% of all VC-containing consumer products. Based on these data, the total number of VC-containing aerosol cans that were not paints or coatings was estimated to be between 0.2 and 0.5 billion cans, or 1.5–3.75% of all aerosol consumer products.

During U.S. Senate hearings conducted in Au- gust 1974 by Senator John V. Tunney before the Environment Subcommittee of the Commerce Com- mittee, Dr. Robert Schaffner of the Food and Drug Administration indicated that VC was not widely used in aerosol consumer products, and was used by only a small percentage of hairspray

1708 Sahmel et al.

manufacturers.(37) A Cosmetic, Toiletry, and Fra- grance Association (CTFA) survey reported that no hairspray product company had manufactured any VC-containing products after June 1973. In the first half of 1973, the CTFA reported that only two com- panies produced any VC-containing products. The total volume produced was reported to be approx- imately 1,625,000 cans, whereas the total hairspray production volume for 1973 was reported to be ap- proximately 450,000,000 cans, for an estimated per- centage of VC-containing cans of less than 0.4%.(38)

A study conducted at the University of Pennsyl- vania reported that VC was present in 1 of 62 aerosol hair products evaluated (1.6%), and in 1 of 168 general aerosol products evaluated (0.6%).(39) Addi- tional data based on EPA studies reported by Brid- bord et al. indicated that vinyl chloride was found in 4 out of 61 aerosol products that were evaluated (6.56%). Bridbord et al. also reported that VC was not a common ingredient of hairspray products, par- ticularly when compared to Freon 11 and 12.(40)

An evaluation of the 1960s and 1970s literature on aerosol science appears to indicate that fluorocar- bon propellants (i.e., propellants 11 and 12, Freon 11 and 12, and P-11 and 12) were far more commonly used than VC in aerosol hairspray products. The Aerosol Handbook found that VC blends were not as popular as other propellant blends in the 1970s, and that the ”standard blend” used in hairsprays dur- ing this time consisted of a mixture of P-12 (53%), P- 11 (36%), and isobutane (11%).(41) A review of The Chemical Formulary book series from the 1950s to the 1970s, which contain data on commercial prod- uct formulas and recipes, demonstrated that aerosol hairspray formulations commonly used during this period appear to have primarily contained propel- lants 11 and 12 only.(42,43) According to a number of articles published in Manufacturing Chemist and Aerosol News, and Aerosol Age, VC was rarely listed as an ingredient of aerosol or hairspray mixtures, and other propellants were mentioned much more fre- quently in the context of current or future products or research.(44−56)

Based on the above detailed literature analy- sis, the fraction of cans of hairspray that potentially contained VC (Fc) was assigned a uniform distribu- tion with a range of 0.4% to 6.56%, with the point estimate set equal to the midrange value of 3.5%. This fraction was used to calculate VC concentra- tions for all salon sizes, although the VC concentra- tion assuming 100% VC-containing hairspray prod- uct use was also calculated for all salon scenarios for comparison.

2.4.2. Duration of Use of VC as a Propellant in Hairsprays (DH)

Some companies selling aerosol hairspray prod- ucts during the 1960s and 1970s produced documen- tation showing that VC was evaluated for potential inclusion in their hairsprays. No documentation or information could be found showing that VC was used as a component of aerosol hairspray products in the United States before 1967. Certain Clairol hairspray products appeared to have used VC as a component of the aerosol propellant from 1967 to 1973.(57) Other hairspray manufacturers did not ap- pear to have begun using VC as a propellant un- til 1968 or 1969, based on information from aerosol hairspray contract filler companies.(58) According to the available information, the date range for the availability of VC-containing hairspray products in the United States (DH) was determined to be 7.25 years, using a starting date of 1967 and an ending date of the spring of 1974, approximately one year after the CTFA reported that all major hairspray companies had removed VC from their hairspray products.(38)

2.4.3. Determination of VC Content in the Hairspray Products (WH)

Hairspray formulation records (provided by Clairol and additional confidential formulation records from other companies) were used to develop a concentration estimate for the likely VC content of hairspray products on the market during the pe- riod of interest. In all available formulation records, VC was incorporated into the products as one com- ponent of a propellant blend that also typically con- tained Propellants 11 and/or 12. The uniform dis- tribution range and midpoint estimate of the VC concentration in these products by weight (WH) was 12.5% for 1967 to 1968, 9.25% for 1969 (range = 6– 12.5%), 8.9% for 1970 to 1972 (range = 5.2–12.5%), and 9.25% for 1973 to April 1974 (range = 12.5– 6%).(41,57) The weighted average of the point esti- mates for the entire 7.25-year period VC was used was 10%, which was consistent with the reported range in The Aerosol Handbook.(41)

2.4.4. Estimated Salon Volume (VF)

There is no systematic research on the size of salons during the 1960–1980 time period. However, between 1996 and 1997, Labreche et al. tabulated floor areas by salon size for 25 salons in Montreal,

Multizone Exposure Modeling: Historical Use of Vinyl Chloride in Hairspray 1709

Canada.(59) For salons with 1–2 stylists, the aver- age floor surface area was 51.8 m2 (range = 21.6– 70.0 m2); for salons with 3–4 stylists, the average floor surface area was 72.1 m2 (range = 25–150 m2); and for salons with 5–9 stylists, the average floor surface area was 100.4 m2 (range = 50.0–130 m2). The salon volumes (VF) were assigned triangular distributions based on these floor area data and a typical commer- cial ceiling height of 2.743 m (9 ft). The above data used in the assessment reflect slightly different vol- umes than those reported in a study of 28 salons by van Muiswinkel et al. where the average salon vol- ume for a salon with 3.5 stylists was 195 m3.(60)

2.4.5. Salon Ventilation Characteristics and Contemporaneous ASHRAE Guidelines (Q’)

Recommended or required air ventilation for an indoor space has been consistently characterized in the literature and in ASHRAE publications in terms of the necessary volume of air introduced over time into a space, most commonly in units of cubic feet per minute (cfm). ASHRAE guidance in the 1960s and 1970s also supports the use of volume of ventilation air per person in an indoor space as a more appropri- ate way to characterize ventilation rather than other measures such as air changes per hour, the value of which is highly dependent upon the size of the space to be ventilated.(61,62)

Typically, the volume of air that is recommended or required for a given space will also be specified per person or per occupant within the space. A ven- tilation text published in 1845 described the need to provide sufficient quantities of fresh air to minimize the possibility of buildup of potentially toxic, foul, or unpleasant concentrations of gases within an indoor space.(63) In this publication, it was determined that at least 10.25 cfm of ventilation air was needed to re- move both bodily scents and exhaled carbon dioxide per person in an indoor space. Additional research done by Yaglou et al. found that a healthy, clean per- son who has recently bathed required 15–18 cfm per person to dilute body odors.(64)

Researchers also recognized from the early part of the 20th century that the volume of space avail- able per occupant is a key variable (along with the temperature of objects in the space) in determining the amount of dilution ventilation needed per per- son. According to Yaglou et al., “with simple venti- lation and with 200 cu ft of air space per person, the air quality was poor to bad when the air supply was under 3 cfm per person, improving rapidly as the air

supply increased to 15 cfm.”(64) The importance of air space per person is also illustrated by the fact that in 1970, ASHRAE recommended a mere 7 cfm of ven- tilation air per person when the air space was 500 cu ft per person, but advised an increase to 25 cfm when the air space was 100 cu ft per person.(65)

The 1964 ASHRAE Guide and Data Book rec- ommended 10–15 cfm per person of ventilation air in commercial areas such as drug stores, grocery stores, or stores with lunch counters. A store with a lunch counter was selected as the best possible comparison with a hair salon because a lunch counter would also need to control both heat generation (i.e., a cook- ing stove versus hair dryers) as well as air contam- inant generation (i.e., cooking odors and smoke vs. hairspray and hair dyes). The 1964 ASHRAE stan- dard also specifically recommended 0.35–0.45 cfm per square foot of space in public buildings. Given the average floor space for the 1–2, 3–4, and 5–9 hairdresser salons presented in Labreche et al. with a maximum of 6, 12, and 27 occupants, respectively (using a total occupant number of three times the number of hairdressers working in a salon, assum- ing one active and one waiting customer per hair- dresser), the standard recommended between 14 and 42 cfm/person.(59)

In 1973, ASHRAE published the first ventila- tion standards for natural and mechanical ventilation in the form of Standard Number 62–73. This stan- dard provided recommended ventilation rates for many different types of public buildings and com- mercial establishments. Specified ventilation flow rates for hair salons included 25 cfm as a mini- mum ventilation rate, with a recommended rate of 30–35 cfm.(62) Table IV includes a summary of key ventilation guidelines, rules, and practices in the 1960s and 1970s.

Additional research has documented a need for published minimum ventilation rates in spaces with retail customers or commercial business visitors. These studies have shown that customers are more sensitive to poor ventilation rates than employees, who tend to become more accustomed to their envi- ronment. As a result, businesses require a minimum level of ventilation in order to ensure the comfort, happiness, and repeat business of their customers. Cain et al. found that for visitors to a particular space, a ventilation rate of “7.5 L/sec per occupant seems necessary to assure 80% acceptance.”(66) This cor- responds to a ventilation rate of 15.9 cfm per occu- pant. Similarly, Berg-Munch et al. found that: “In a space occupied by sedentary persons, a steady-state

1710 Sahmel et al.

Table IV. U.S. Ventilation Guidelines, Rules, and Practices in the 1960s and 1970s (61,62,65)

Year Published Information Given Notes Publication

1964 10–15 cfm per person Includes guidelines for retail stores (not specific to salons)

ASHRAE Guide and Data Book, Chaps. 18–19, pp. 235–252, American Society of Heating, Refrigerating, and Air Conditioning Engineers; Atlanta, GA, 1964.

1964 0.35–0.45 cfm per square foot Section about public buildings (assuming 15 ft. by 20 ft. and 8 people, range becomes 13.125–16.875 cfm per person)

ASHRAE Guide and Data Book, Chaps. 18–19, pp. 235–252, American Society of Heating, Refrigerating, and Air Conditioning Engineers; Atlanta, GA, 1964.

1970 15–18 cfm for healthy, clean person to simply dilute body odor

Does not include additional ventilation required to address nonhuman sources of compounds released to indoor air

Klauss, AK; Tull, RH; Roots, LM; Pfafflin, JR. History of the Changing Concepts in Ventilation Requirements. ASHRAE Journal, June 1970; pp. 51–55.

1973 Minimum rate of 25 cfm per person and recommended rate of 30–35 cfm (hair salons)

First standard to include a guideline specific to salons

ASHRAE Standards for Natural and Mechanical Ventilation, 62–73, American Society of Heating, Refrigerating, and Air Conditioning Engineers; Atlanta, GA, 1973.

ventilation rate of 8 L/sec per person is required in order to satisfy 80% of people entering the space (visitors). People remaining in the space (occupants) are less dissatisfied than the visitors are.”(67) This equates to a ventilation rate of 16.9 cfm per occupant.

In this study, the total flow rate for each salon (Q) was calculated by multiplying the maximum es- timated occupancy (three times the number of hair- dressers) by the recommended ASHRAE unit flow rate (Q’) of 25 cfm per person for hair salons, which is likely to have been necessary to dilute the air con- centrations of hair products used and the heat from the dryers, as well as for general customer and stylist comfort.(61,62,65) A minimum airflow rate of 15 cfm per person was selected for a business establishment such as a salon based on the literature reviewed. A triangular distribution with the full range of 15– 35 cfm per person was adopted in the sensitivity analysis.

2.4.6. Mass of Hairspray Applied per Customer (ME)

A study in the trade publication of CTFA, the Cosmetic Journal, evaluated beauty salon air qual- ity by measuring average hairspray use by mass per

customer during a typical day in a salon during the early 1970s. The mass of hairspray used per customer (ME) was determined by measuring the weight differ- ence for all cans of hairspray used in a given day, and resulted in a calculated range of 6.3–16.3 grams of hairspray use per customer. A triangular distribution with this measured range was used for the sensitivity analysis, and a point estimate of 12 was used based on the average of the measured data. The usage mass is unlikely to be appreciably affected by the type of pro- pellants used, and data based on non-VC propellants such as isobutane/fluorocarbon mixtures were con- sidered representative of hairsprays containing VC.

2.4.7. Hairspray Generation Rate (GH)

The average of mass generation rates represent- ing variation between full and empty containers was determined from reported data.(68) Long-term aver- age exposure was not expected to be sensitive to this parameter because as the can empties, longer spraying times are required to apply the same mass, which affects the peak concentration, but not cu- mulative long-term average exposure. A triangular distribution with a mode of 34 grams per minute (g/min) and range of 18–46 g/min was assigned.

Multizone Exposure Modeling: Historical Use of Vinyl Chloride in Hairspray 1711

2.4.8. Probability of a Hairspray Event per Increment of Time (Pr[E])

To realistically assess transient hairspray usage in a salon, the probability of a salon worker spray- ing hairspray for 15-minute intervals throughout the work day (Pr[E]) was conceptualized as a series of Bernoulli trials. The 95% upper confidence probabil- ity of a hairspray event occurring during a 15-minute interval was calculated using 12 days of contempo- raneous customer data presented in Hoffman repre- senting both winter and summer months.(27) The re- sultant probability of 0.296 per 15-minute period, or a 29.6% chance that a salon worker will be spray- ing hairspray during a 15-minute time interval during the work day, corresponds to an expected value of customers per stylist (EW) of 9.5 customers per day and expected value of customers summed across all co-workers of 9.5–76 depending on salon size. This probability also corresponded to the range used in our probabilistic assessment (e.g., 5–14 customers per day).

2.4.9. Random Air Speed (S)

Random air speed (S) was estimated using data from Baldwin and Maynard, which indicated that a value of 0.1 m/sec was typical for offices and stores.(69) This range is consistent with Nicas where a range of 0.05 m/sec (3.1 m/min) to 0.25 m/sec (15 m/min), and a most likely value of 0.15 m/sec (9.1 m/min), was used for an indoor space and as- sessment of exposure from use of a parts washer.(29)

Similarly, Leino et al. reported mean air speeds of 0.09 m/sec (5.4 m/min) and 0.13 m/sec (7.8 m/min) for small (n = 10) and large (n = 10) Finnish hairdress- ing salons, respectively.(70) A triangular distribution with a range of 3 to 12 with a mode of 6 m/min was therefore used for this parameter.

2.4.10. Residential Air Exchange Rate (AR) and Room-to-Room Air Exchange Rate (ARTR)

In 1988, Nazaroff aggregated the two largest U.S. studies containing air exchange rate data up to that time. One study consisted of 1,048 tracer gas mea- surements in 266 low-income dwellings across 14 cities and the second study consisted of November to March measurements of 312 homes with a me- dian age of less than 10 years. The distribution was aggregated (geometric mean = 0.68, geometric stan- dard deviation = 2.01) in an attempt to best represent

the U.S. mixture of “leaky” homes and more energy- efficient modern structures. The arithmetic mean of 0.87/hr, based on a log normal distribution assump- tion, was used as the point estimate and the full dis- tribution was used in the sensitivity analysis.(71)

The room-to-room salon air change rate (ARTR) required in the three-zone model (i.e., air exchange between salon zone 2 and rest of home zone 3) was estimated based on ASHRAE 62-1973 guidelines for airflow in residential kitchens and three assumed oc- cupants. The range of calculated room-to-room air change rates was 1.5–6.4. Room-to-room air change rates between 3 and 6 per hour for U.S. EPA test home data cited in the indoor air quality RISK model documentation are considered typical.(72)

3. RESULTS

3.1. Transient Two-Zone Model Results

The point estimate of the transient two-zone model daily TWA exposure using a market share estimate of VC-containing hairsprays (range of 0.4– 6.6% of products used) for the small, medium, and large salons was 0.18 ppm, and for a residential salon was 0.03 ppm. For the scenario in which all hairspray products used were assumed to contain VC, the point estimates of the TWA exposure for the commercial salons were 5.0–5.1 ppm, and for the residential sa- lon was 0.9 ppm (Table V). Cumulative exposure es- timates were then calculated assuming a potential ex- posure time of 8 hours per day, 5 days per week, and 50 weeks per year over a time duration of 7.25 years as discussed above under market availability of VC-containing hairsprays. The point estimate for cu- mulative exposure assuming a market share estimate of VC-containing hairsprays was 1.28–1.30 ppm-year for small, medium, and large salons, and 0.66 ppm- years for the home salon scenario. For the scenario in which only VC-containing hairspray products were used, the cumulative dose was 37 ppm-year for the commercial salons and 19 ppm-year for the residen- tial salon (assuming 7.25 years of possible exposure). Fig. 3 illustrates exposure patterns over time, both for the near field and far field, and for the full day compared with a typical 30-minute period. It should be noted that breathing rates were not taken into account when calculating cumulative exposure esti- mates because OSHA and other regulatory agencies make the assumption for the purposes of conserva- tive estimates that the same concentration found in the breathing zone is actually inhaled, and that 100%

1712 Sahmel et al.

Table V. Summary of Key Model Results: TWA Concentration, TWA Point Estimates, and Cumulative Exposure Estimates

Location

Calendar Years of Exposure

Occupational Equivalent Years

of Exposure

TWA Averaging

Time (Hours)

Point Estimate

TWA – (ppm) Mean

Upper Bound

Cumulative Point Estimate

Exposure (ppm-year)

Mean Upper Bound

Market Fraction of Products Used (0.4–6.56%) Contain VC Residential salon 7.25 21.75 24 0.03 0.05 0.13 0.66 1.0 2.8 Small commercial

salon 7.25 7.25 8 0.18 0.16 0.28 1.28 1.2 2.0

Medium commercial salon

7.25 7.25 8 0.18 0.17 0.27 1.29 1.2 2.0

Large commercial salon

7.25 7.25 8 0.18 0.17 0.27 1.30 1.2 2.0

All Products Used (100%) Contain VC Residential salon 7.25 21.75 24 0.9 1.4 3.6 19 30 79 Small commercial

salon 7.25 7.25 8 5.0 4.7 7.4 37 34 54

Medium commercial salon

7.25 7.25 8 5.1 4.7 7.1 37 34 52

Large commercial salon

7.25 7.25 8 5.1 4.9 7.2 37 35 52

Fig. 3. Predicted daily airborne VC time-concentration profile in a large salon for a typical iteration of the probabilistic model assuming all hairspray products were formulated with VC. The near field (NF) represents a hairdresser’s personal breathing zone exposure and the far field (FF) represents ambient levels of VC in the salon including co-worker VC releases. Large peaks (>50 ppm) correspond to worker hairspray events affecting NF breathing zone, whereas small peaks (<25 ppm) represent co-worker hairspray events contributing to FF ambient VC levels in the salon. Hairspray events are randomly distributed in the model in 15-minute increments such that individual small peaks can include the contribution of multiple co-workers.

of this inhaled dose is ultimately absorbed. How- ever, the average quantity of VC retained in human lung tissue has been observed to be approximately 42%.(73,74)

In the sensitivity analysis, input distributions were considered for salon airflow rate, residential air exchange rate, random air speed, salon or home volume, VC weight content, probability of having a customer per 15-minute period, mass of hairspray applied per customer, and percentage of hairspray

products that contained VC (Table III). The 95th percentile (upper bound) TWA concentration for the small, medium, and large salons from the Monte Carlo analysis was 0.3 ppm, and for the home salon scenario was 0.1 ppm. The 95th percentile of cumu- lative exposure for the small, medium, and large sa- lon scenarios was 2.0 ppm-years, and for the home salon was 2.8 ppm-year. For the scenario in which all hairspray products used were assumed to con- tain VC, the 95th percentile of cumulative exposure

Multizone Exposure Modeling: Historical Use of Vinyl Chloride in Hairspray 1713

Table VI. Summary of Results: Sensitive Parameters

Small Medium Large Residential Commercial Commercial Commercial

Parameters Considered in Sensitivity Analysis Salon Salon Salon Salon

Probability of a customer per 15-minute period –Worker 9.6% 12.1% 5.7% 3.3% Probability of a customer per 15-minute period –Co-worker Not applicable 6.7% 6.8% 5.0% Fraction of products containing VC 8.8% 31.0% 35.1% 34.1% Weight content of VC VC 0.9% 2.8% 4.3% 3.8% Salon airflow rate (cfm/person) Not applicable −15.2% −16.1% −19.6% Random air speed (m/sec) −1.5% −1.8% −1.5% −1.6% Salon/home volume (m3) −23.8% 0.0% −0.5% 0.0% Residential air change rate (ACH) −48.7% Not applicable Hairspray generation rate (g/s) −0.1% 0.0% 0.0% 0.0% Amount of hairspray used (g/customer) 6.6% 30.2% 30.1% 32.6%

100% 100% 100% 100%

for the commercial salon scenarios was 52–54 ppm- year, and for the residential salon was 79 ppm-year (Table V). Parameters contributing at least 1% to the variance in cumulative exposure included: probabil- ity of a customer per 15-minute period, the fraction of products containing VC, the weight content of VC in a hairspray product, salon airflow rate, and mass of hairspray used per customer (Table VI). For each of these parameters, published literature was available to develop reliable point estimates. The 95th per- centile cumulative exposure calculations were within a factor of 3 of the mean, or central tendency, ex- posure, which illustrates that knowledge of the pre- cise values for each of the various parameters is not necessary in order to accurately estimate, with confi- dence, the likely true concentration (that is, sensitiv- ity is not a great concern).

Table VII presents some of the other interesting outcomes from the transient two-zone model. The highest instantaneous peak estimated for all three

professional salon scenarios was 134–135 ppm with a 95th percentile of 207 ppm. The highest 15-minute TWA estimate was 12–14 ppm with a 95th percentile of 17–20 ppm. Finally, the ratio of breathing zone to room airborne VC concentrations of 1.2–1.3 for com- mercial salons was similar to the ratio of personal to area concentration of 1.4 calculated from ethanol data reported in van Muiswinkel et al. for Dutch salons.(60)

3.2. Residential Multizone Model Comparison

The two-zone model was used for the residen- tial setting because of typical residence ventilation characteristics and the fact that room-to-room air exchange is far higher than the air exchange rate for the entire residence. For room air change rates between 3 and 6 per hour (typical of U.S. EPA test home data cited in the indoor air quality RISK model documentation), predicted breathing zone

Table VII. Summary of Additional Model Results: Ratio of Near-Field to Far-Field Concentrations, Air Change Rate Estimates, Peak Exposures

Ratio of Worker Breathing Zone (Personal) to Room

(Area) Concentration (Unitless)

Estimated Air Change Rate (Calculated from

cfm/Person Parameter for Commercial Locations)

Highest 15-Minute TWA

(ppm)

Highest Instantaneous Peak (ppm)

Number of Upper Lower Upper Upper Upper Location Stylists Mean Bound Bound Mean Bound Mean Bound Mean Bound

Residential salon 1 1.4 2.2 0.2 0.9 2.1 9 18 126 200 Small commercial salon 2 1.2 1.3 1.3 2.0 3.2 14 20 135 207 Medium commercial salon 4 1.2 1.3 1.3 2.5 4.5 12 18 134 207 Large commercial salon 9 1.2 1.3 3.0 4.6 6.9 12 17 135 207

1714 Sahmel et al.

concentrations were less than a factor of 1.05–1.2 larger than those predicted by the two-zone model that confirmed that the interzonal airflow rate (β) is the key limiting parameter (Table VIII).(72)

3.3. Steady-State Imperfect Mixing Model Comparison

Estimates of the daily average airborne con- centration of VC based on the steady-state imper- fect mixing model were consistent with the tran- sient two-zone model (Table IX, Fig. 4). Cumulative exposure estimates were 0.73 ppm-years for the res- idential salon, 1.3 ppm-years for the small salon, 1.4 ppm-years for the medium-sized salon, and 1.3 ppm-years for the large salon scenario. Short-term peaks or 15-minute average airborne concentrations cannot be estimated using the steady-state model.

3.4. Model Evaluation

Contemporaneous airborne concentration data for hairspray propellant components were col- lected in 1972 at the Central Beauty Salon by Hoffman and are suitable for model comparison. The characteristics of this salon included 10 stylist stations, 28 chairs, and 21 dryers.(27) The air ex- change rate was 6 to 8 per hour with an average duct airflow rate (including recycled air) of 2,060 cfm (equal to duct cross-sectional area multiplied by face velocity). The hairspray usage rate was 6– 16 g/customer and two propellant blends were used including P-12/P-11/Isobutane (w/w: 43%/48%/9%) and P-12/P-11/Methylene Chloride/Isobutane (w/w: 42%/31%/19%/8%). The weight content of the pro- pellant in the hairsprays was 50%. Probabilistic model estimates were prepared for propellants P- 11 and P-12 using the following parameters from the Hoffman study: daily customers (11 stylists av- eraging 104 customers/day), air exchange rate (6 to 8 hr−1 paired with an estimated effective vol- ume of 225–275 m3), hairspray usage rate (6–16 g/customer), and propellant component weight con- tent (16–24%). The estimated average P-11 and P- 12 concentrations using the model described in this study were within a factor of 1.8 of the measured data reported in Hoffman (Fig. 5).(27) Nicas et al. showed that for a similar two-zone model appli- cation, the modeled benzene concentrations were also within a multiplicative range of one-half to two-fold the measured concentrations determined through a simulation study.(29) The underprediction

of the model in the summer months is likely at- tributable to the greater rate of air recirculation that reduces the effectiveness of dilution ventila- tion and was difficult to estimate from the informa- tion provided by the author. Additionally, although the sampling plan used by Hoffman included mea- surement of both hourly background samples and peak samples collected immediately after hairspray events, the samples were all collected using a can- ister grab sampling method. At the time the study was conducted in the early 1970s, the authors con- sidered this method more robust than sampling us- ing a continuous monitoring instrument, since instru- mentation during that era did not provide a specific quantitative result for the air contaminants of inter- est. However, this sampling method may still have af- fected the consistency of the results and the resulting certainty in the study outcomes.

Other studies reporting indoor propellant concentrations are consistent with Hoffman (Table X).(27) Peak concentrations greater than 100 mg/m3 occur, but full-shift TWA average concentrations of propellants are typically 0.1–60 mg/m3 (typical propellants in aerosol hairsprays include ethanol, propane, isobutane, Propellant 11, Propellant 12, butane, and dimethylether). Ethanol is frequently reported in studies of hair salons because it is a common solvent used in many salon products, including hairsprays, and is considered to be an indicator for solvent exposure in salons in general.(59,60,75) In hair styling products such as gels, lotions, emulsions, and sprays, the concentration of liquid ethanol in the solution may be 50–90% (w/w).(70) VC was formulated at lower weight con- tents in hairspray (i.e., ≤15% w/w) than ethanol and was not used in gels, lotions, or emulsions. As a result, it would be present at lower airborne concen- trations than the ethanol concentrations reported in Table X.

3.5. Comparison to Acceptable Cumulative Exposure Levels Identified by OSHA and ACGIH

These cumulative exposure estimates were com- pared against the current OSHA PEL for VC as well as the ACGIH TLV for VC (Fig. 1). The PEL and TLV for VC are both currently set at 1 ppm as an 8- hour TWA exposure. Assuming exposure to 1 ppm is an acceptable airborne concentration for workers for a 40-hour work week, this corresponds to an ac- ceptable lifetime dose of 40–45 ppm-years, which is

Multizone Exposure Modeling: Historical Use of Vinyl Chloride in Hairspray 1715

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lu m

e of

V F

= 35

6 m

3 an

d ne

ar -fi

el d

he m

is ph

er e

R N

= 0.

78 m

in ra

di us

. e U

.S .E

P A

te st

ho m

e ex

pe ri

m en

ts in

di ca

te th

at un

de r

ty pi

ca lc

on di

ti on

s na

tu ra

lr oo

m -t

o- ro

om ai

rfl ow

is at

le as

tt hr

ee ro

om ai

r ch

an ge

s pe

r ho

ur .

1716 Sahmel et al.

Table IX. Comparison of Point Estimates to Uncertainty Analysis for Market Fraction of VC-Containing Products Used (0.4– 6.56%)

Point Estimate: Steady-State Mixing Model

Sensitivity Analysis : Two-Zone Model Cumulative Exposure

Point Estimate: Transient Two-

Zone Model Mixing Factor Concentration Mean Upper Bound Location (ppm-Year) (Unitless) (ppm-Year) (ppm-Year) (ppm-Year)

Residential salon 0.66 0.625a 0.73 1.03 2.78 Small commercial salon 1.28 0.714b 1.33 1.18 2.01 Medium commercial salon 1.29 0.476c 1.40 1.20 1.95 Large commercial salon 1.30 0.385d 1.31 1.23 1.96

aMixing factor of 0.625 based on Cherrie (1999) modeled worker NF to FF conc. ratio of 1.6 for V = 300 m3, ACH = 1, and β = 10 m3/min. bMixing factor of 0.714 based on Cherrie (1999) modeled worker NF to FF conc. ratio of 1.4 for V = 100 m3, ACH = 1–3, and β = 10 m3/min. cMixing factor of 0.476 based on Cherrie (1999) modeled worker NF to FF conc. ratio of 2.1 for V = 100 m3, ACH = 1–3, and β = 10 m3/min. cMixing factor of 0.385 based on Cherrie (1999) modeled worker NF to FF conc. ratio of 2.5 for V = 300 m3, ACH = 3, and β = 10 m3/min.

Fig. 4. Comparison of point estimate of VC exposure to the probabilistic mean of the cumulative exposure estimates from the uncertainty analysis for the scenario in which a market fraction (0.4–6.56%) of products used contain VC.

20–35 times higher than the calculated estimate of the cumulative lifetime dose of 1.3 ppm-years (with a 95th percentile of 2.0 ppm-years). When comparing the OSHA acceptable lifetime dose to the scenario in which only VC-containing hairsprays were used, the cumulative dose associated with VC exposure was 37 ppm-years, which although far higher, was still below the 40–45 ppm-year estimate (assuming 7.25 years of exposure). However, at the 95th percentile, this scenario produced estimates above the OSHA acceptable lifetime dose (52–54 ppm-year for the

commercial salons and 79 ppm-year for the home salon).

4. DISCUSSION The results of this study illustrate the capacity of

appropriately selected models to characterize com- plex exposure generation rate and decay rate sce- narios if the model input parameters are sufficiently robust. The correlation between modeled concen- trations and measured concentrations of airborne hairspray propellants used in hair salons during the

Multizone Exposure Modeling: Historical Use of Vinyl Chloride in Hairspray 1717

Fig. 5. Comparison of model estimates to contemporaneous measured airborne propellant concentrations at a large salon with 10 operator stations.

Table X. Survey of Measured Airborne Concentrations of Propellant Components in Hairspray (27,59,60,70,75,91)

Components

Flourocarbon 12 Flourocarbon 11 Methylene Reference Notes (Freon 12) (Freon 11) Chloride Et OH

Labreche et al., 2003

26 salons; personal sampling; avg. 8 hr TWA

– – – 40 mg/m3 (range: 0.17–447 mg/ m3)

Hollund and Moen, 1998

Area sampling – – – 33.3 mg/m3 w/o ventilation; 9.5 mg/m3

w/ventilation

1–2 minute “peak” concentrations during release of pollutant

20–1580 mg/m3 5.6–1010 mg/m3 <3.5–451 mg/m3 8–491 mg/m3

Hoffman, 1973 Daily concentration: Table VII: Summer

20–64 mg/m3 11–56 mg/m3 – 17–55 mg/m3

Daily concentration: Table VIII: Winter

5–25 mg/m3 6–28 mg/m3 <3–7 mg/m3 8–21 mg/m3

Kersemaekers, 1998

Presence or absence of ventilation device predictive of exposure grouping; avg. 8 hr TWA

– – – w/ventilation: 7.4 mg/m3

– – – w/o ventilation: 17.4 mg/ m3

Ventilation determined based on – – – Leino, 1999 whether subjects experienced

discomfort; peak total VOC (not specific to ethanol)

– – – 45 mg/m3

van Muiswinkel et al., 1997

33 salons; seasonal range; 8hr TWA

– – – 0.1–57 mg/m3

time period of interest underscores the utility of the transient two-zone model to predict TWA concentra- tions for various occupational and consumer use sce- narios. Additionally, the results of the steady-state model demonstrate the successful application of a

simple screening model to replicate the results of a more precise but parameter-intensive higher tier model, increasing confidence that the results of the analysis are not highly dependent on the type of model selected.

1718 Sahmel et al.

Our analysis indicates that potential exposures to VC through the occupational use of hairsprays in home salons or professional hair salons during the 1960s–1970s was not likely to have been suf- ficient to cause or increase the risk of developing HAS. When employing the assumption that only VC- containing hairsprays were used in a salon, 95th per- centile TWA concentration estimates were found to be in the range of 7–8 ppm for all three professional salon scenarios. Such concentrations correspond to a theoretical lifetime cumulative dose of 37 ppm- years, with a 95th percentile upper bound of 52–54 ppm-years, assuming 7.25 years of possible exposure. Considering the lowest reported cumulative expo- sure in the published literature associated with a case of HAS (288 ppm-years) and the finding of no in- crease in relative risk for HAS below 500 ppm-years of cumulative exposure, the findings suggest that the potential for exposure to VC from hairspray use in the United States would not be sufficient to lead to HAS.(18) These results are also consistent with the epidemiology literature for hair stylists, which does not show an increased incidence of HAS or any other liver tumors among hair stylists or employees of hair salons during the time period of interest.(20−24) Our assessment of the health risk is also consistent with the PBPK analysis of Reitz et al., who compared the delivered VC dose at various concentrations with the incidence of HAS.(14)

It was also found that the volume of the space evaluated had only a minimal effect on the estimated airborne concentrations of VC. This was true even with the use of a wide range of possible ventila- tion rates in the sensitivity analysis. As mentioned in some texts, for commercial spaces, ventilation, as characterized by volumetric airflow, was far more im- portant in predicting concentrations over an 8-hour work day than the size of the room. This is consistent with historical and current ventilation guidelines that emphasize occupancy-dependent airflow rates rather than target air exchange rates. In contrast, in residen- tial spaces where air flow tends to be induced by ther- mal gradients and wind flow rather than mechanical ventilation, home volume was found to be a sensitive parameter.

The Monte Carlo analysis indicated that the 95th percentile estimate of airborne concentration (and dose) was only a factor of 2 higher than the point estimate. In this assessment, home volumes as low as 113 m3 (3991 ft3) and air change rates as low as 0.08 ACH were considered. These values are poten- tial outliers because they are extremely low, and this

positively skewed the mean probabilistic result rela- tive to the point estimate when a 24-hour averaging time was considered.

In addition to the salon studies considered in this analysis, two early 1970s studies assessed VC in hair- spray. Gay et al. evaluated potential VC concentra- tions following a single 30-second or 60-second hair- spray event in three rooms of different volumes: a simulated home bathroom, an office room, and a public restroom.(76) In the study, the authors col- lected short-term (2 minute) area samples at differ- ent time periods of slightly more than 2 hours. The ventilation and hairspray usage rates were not mea- sured. None of the scenarios evaluated described the use of hairspray in a salon by professional hair- dressers, and the study was conducted under re- stricted ventilation conditions (e.g., closed vents, windows, passageways, and doors) that limited the applicability of the reported measurements to con- ditions in a typical hair salon. In spite of these differ- ences, the Gay et al. measurement results are consis- tent with the concentration profile predicted by the two-zone model for a discrete release of hairspray when the generation rate, weight content, and ven- tilation conditions are considered.

A second study by Bridbord et al. evaluated exposure to halogenated hydrocarbons; however, with respect to hairspray, the authors reported the data from the Gay study.(40) In addition to these studies, the Netherlands National Institute for Pub- lic Health and the Environment (RIVM) default hairspray scenario for the ConsExpo 4.1 Consumer Exposure and Uptake Models was evaluated for potential use in this study.(77) Although the RIVM default parameters were considered in this as- sessment, the ConsExpo 4.1 experimentally cal- ibrated spray model is intended to character- ize very low volatility or nonvolatile compounds and is not appropriate for volatile compounds or gases.

The strength of this modeling effort would have been improved had there been reliable VC measure- ments against which the modeling results could have been compared. However, given the number of pub- lished studies that have measured similar airborne contaminant concentrations in hair salons, the results appear to be precise and reliable.(59,60,75) The P-11 and P-12 data from Hoffman were useful for model evaluation, since the vapor pressures for the hair- spray propellants P-11, P-12, and VC of 0.9, 5.7, and 3.3 atm, respectively, reflect the similar volatility of these compounds.(27)

Multizone Exposure Modeling: Historical Use of Vinyl Chloride in Hairspray 1719

The duration of use of VC as a propellant in hair- spray was based on available company documenta- tion, published literature, and a personal interview with an individual who was integrally involved in the manufacture of hairsprays during the period of inter- est. Although it is believed that a realistic parameter of 7.25 years was used (including an additional year to account for previously purchased VC-containing hairspray product inventory at salons), it is possible that VC may have been used in some hairspray prod- ucts before 1967. In this case, the concentration es- timates presented would not be affected, but cumu- lative exposure values might change. Additionally, the fraction of products containing VC evaluated in this study was specific to the U.S. market. Companies in Germany, for example, appear to have used VC- containing propellants in aerosol products, including hairsprays, earlier (1950s) and in greater quantities than in the United States.(78) Because the fraction of hairspray products containing VC was the most sen- sitive factor for all commercial salons, and because the data used to evaluate this parameter were spe- cific to the United States, an analysis of a scenario in which all the hairspray products used in a salon con- tained VC was an important consideration and key part of this study. At the 95th percentile of cumula- tive exposure estimates assuming the use of only VC- containing hairsprays (for all salon scenarios), the estimated cumulative exposures were approximately one-fourth of the lowest cumulative lifetime dose as- sociated with HAS and less than one-fifth of the cu- mulative dose identified in prior studies showing an increased risk of HAS.(14,18) Although this scenario is probably relatively unlikely given the small frac- tion of VC-containing hairsprays that appeared to be available in the United States, it demonstrates that even exclusive use of VC-containing hairspray prod- ucts during the time period of interest might not be expected to have resulted in sufficient exposure to in- crease the risk of HAS, under a wide range of oper- ating conditions for hair salons, and for similar dura- tions of use.

The model equations used in this study are likely to be applicable to a wide range of scenarios in which the generation and decay rates and associated concentrations of volatile substances in an enclosed space are of interest. The use of multiple zones may be helpful to better understand the differences (or lack of differences) in concentrations at progressively greater distances from the generation source when information about ventilation rates and other impor- tant parameters is known or can be characterized

with confidence. The uncertainty analysis was also a critical part of this study and demonstrated the pos- sible range of model estimates given variability in the model parameters. Finally, a source of evaluation data (in this case, propellant measurements from a working hair salon) was critical to understanding the capabilities of the models used.

ACKNOWLEDGMENTS

The authors are grateful to Clairol for providing formulation details and other available information regarding hairspray products during the time period of interest. The authors are also grateful to Mont- fort Johnsen for the information he provided via per- sonal interview. The original research upon which this study is based was funded by multiple compa- nies involved historically in the production of VC and VC-containing products. None of the companies that funded the original research reviewed the article prior to submission. One of the authors has served as an expert witness in litigation related to work- place exposures to VC. Cited references are avail- able upon request from the corresponding author. The authors would like to thank Matthew Ground for his assistance in preparing this article, as well as Pamela Williams for her research contributions while employed by ChemRisk.

APPENDIX A: MODEL SYMBOLS

The symbols and abbreviations below are used in the exposure model provided in Appendix B and dis- cussed in the text. The units are indicated in paren- thesis.

Abbreviations

CW Co-worker(s) E Event F Far field N Near field O Occupants W Worker H Hairspray R Residential

Indices

a zone a—three-zone model b zone b—three-zone model i parameter i—two-zone dynamic model j 15-minute period j

k stylist k

1720 Sahmel et al.

Symbols

AR residential air change rate (hr−1) ARTR residential room-to-room air

change rate (hr−1) AC commercial air change rate (hr−1)

β interzonal airflow rate (m3/min) C1 concentration in zone 1—three-

zone model (mg/m3) C2 concentration in zone 2—three-

zone model (mg/m3) C3 concentration in zone 3—three-

zone model (mg/m3) CE cumulative exposure (ppm-year)

CN(Tp, j ) near-field concentration for event initiated period j after TP minutes (ppm)

CF(Tp, j ) far-field concentration for event initiated period j after TP minutes (ppm)

CTOTAL,N(TS) total near-field concentration summed across all events at time TS (ppm)

CTOTAL,F(TS) total far-field concentration summed across all events at time TS (ppm)

CTWA,N[t1,t2] time-weighted average near-field concentration between time t1 and t2 (ppm)

CTWA,F[t1,t2] time-weighted average far-field concentration between time t1 and t2 (ppm)

DH number of calendar years of hair- spray usage (years)

ECW number of co-worker hairspray events per day; this is a proba- bilistic value dependent on Pr[Ej = k | n]

EW number of worker hairspray events per day; this is a probabilistic value dependent on Pr[E]

Ej,w, number of worker hairspray events in period j

Ej,cw, number of co-worker hairspray events in period j

fi secondary intermediate parameter i of dynamic two-zone model

FC fraction of cans containing vinyl chloride

GE worker vinyl chloride mass gen- eration rate during spray event (mg/min)

GH hairspray generation rate during spray event (g/min)

Gcw,day daily co-worker(s) vinyl chlo- ride mass generation rate during (mg/day)

Gw,day daily worker vinyl chloride mass generation rate during (mg/day)

k imperfect mixing factor (unitless) λi primary intermediate parameter i

of dynamic two-zone model ME hairspray usage rate during a single

hairspray event (g/customer) NCW number of co-workers

NO number of occupants in salon NP number of 15-minute periods per

day OE occupational equivalent years

(years) Pr[E] probability of a hairspray event in a

15-minute period for one stylist Pr[Ej = k | n] probability of k hairspray events in

a 15-minute period given n stylists Qab airflow from zone a to zone b—

three-zone model (m3/day) Q’ unit ventilation rate (m3/min/

occupant) Q salon ventilation rate (m3/min)

RN radius of near-field hemisphere (m) S random air speed (m/min) t time (min)

TP,j time elapsed since initiation of hair- spray event in period j (min)

TE duration of single hairspray event (min)

TS time elapsed since beginning of shift (min)

TW length of work day or exposure pe- riod (min)

VN near-field volume (m3) VF far-field volume (m3) VS salon volume—residential three-

zone model (m3) VR rest of home volume—residential

three-zone model (m3) WH vinyl chloride content in hairspray

(g/g)

Conversion factors

CF1 2.56 mg/m3 per ppm for vinyl chloride at standard temperature and pressure

CF2 1,000 mg/g

Multizone Exposure Modeling: Historical Use of Vinyl Chloride in Hairspray 1721

CF3 60 min/hour CF4 24 hour/day

APPENDIX B: MODEL FORMULATION

Transient Two-Zone Model

In the model below, separate equations are used to describe the transient concentration profile during and after each spray event. The total exposure pro- file is calculated by superimposing the concentration profile for each individual event and consideration of the fraction of products containing VC.

VC generation rate:

GE = GHWHCF2 Duration of single hairspray event:

TE = MEGH Interzone airflow rate (β) and near-field volume:

β = 1 2

( 4π(RN)2

)(1 2

S )

VN = 12 (

4 3 π(RN)3

)

Ventilation rate:

Q = Q′No

Q = ARVF CF3

AC = Q · CF3VF Probability of k hairspray events in 15-minute

period j given n stylists:

Pr[Ej,cw = k | n] = ⎛ ⎝ n

k

⎞ ⎠ Pr[E]k(1 − Pr[E])(n−k)

Pr[Ej,w = 1 | n = 1] = Pr[E] Number of hairspray events per day at salon:

NP = TW/(15 min)

ECW = NP∑ j=1

Ej,cw

EW = NP∑ j=1

Ej,w

Expected value [EW+ECW] =NpPr[E] + Np∑NCW k=1 ·k( nk )Pr[E]k(1 − Pr[E])(n−k).

Near-field and far-field concentration during spray event for generation rate GE (mg/min) for time 0 ≤ Tp,j ≤ TE:(28)

CN(Tp, j ) = [ f1 + f2 exp(λ1Tp, j ) + f3 exp(λ2Tp, j )]

CF1

CF(Tp, j ) = [ f6 + f7 exp(λ1Tp, j ) + f8 exp(λ2Tp, j )]

CF1 where:

λ1 = 0.5 [

− (

β × VF + VN(β + Q) VN × VF

)

+ √(

β × VF + VN(β + Q) VN × VF

)2 − 4

( β × Q

VN × VF

)]

λ2 = 0.5 [

− (

β × VF + VN(β + Q) VN × VF

)

− √(

β × VF + VN(β + Q) VN × VF

)2 − 4

( β × Q

VN × VF

)]

f1 = GE/Q + GE/β

f6 = GE/Q

f2 = GE (

β × Q + λ2 × VN(β + Q) β × Q × VN(λ1 − λ2)

)

f3 = −GE (

β × Q + λ1 × VN(β + Q) β × Q × VN(λ1 − λ2)

)

f7 = GE ( λ1 × VN + β

β

)( β × Q + λ2 × VN(β + Q)

β × Q × VN(λ1 − λ2) )

f8 = −GE ( λ2 × VN + β

β

)( β × Q + λ1 × VN(β + Q)

β × Q × VN(λ1 − λ2) )

Near-field and far-field concentration after spray event for generation rate G (mg/min) for time Tp,j > TE:(28)

CN(Tp, j ) = [ f4 exp(λ1[Tp, j − TE]) + f5 exp(λ2[Tp, j − TE])]

CF(Tp, j ) = [ f9 exp(λ1[Tp, j − TE]) + f10 exp(λ2[Tp, j − TE])]

1722 Sahmel et al.

where:

CN,t ′ = CN(TE)

CF,t ′ = CF(TE)

f4 = (

β(CF,t ′ − CN,t ′) − λ2 × VN × CN,t ′ VN(λ1 − λ2)

)

f5 = (

β(CN,t ′ − CF,t ′) + λ1 × VN × CN,t ′ VN(λ1 − λ2)

)

f9 = (

λ1 × VN + β β

)

× (

β(CF,t ′ − CN,t ′) − λ2 × VN × CN,t ′ VN(λ1 − λ2)

)

f10 = (

λ2 × VN + β β

)

× (

β(CN,t ′ − CF,t ′) + λ1 × VN × CN,t ′ VN(λ1 − λ2)

)

Concentration as a function of time TS (superpo- sition of contribution all current and past 15-minute events):

CTOTAL,N(TS) =

⌈ TS 15

⌉∑ j=1

FC(Ej,wCN(TS−15[ j−1])

+ Ej,cw CF(TS−15[J−1]) )

CTOT AL,F(TS) =

⌈ TS 15

⌉∑ j=1

FC(Ej,wCF(TS−15[ j−1])

+ Ej,cw CF(TS−15[J−1]) )

Time-weighted average concentration:

CTWA,N[t1,t2] = 1

t2 − t1

∫ TS=t2 Ts=t1

CTOT AL,NF(TS)dTS

CTWA,F[t1,t2] = 1

t2 − t1

∫ TS=t2 Ts=t1

CTOT AL,NF(TS)dTS

Occupational equivalent cumulative exposure assuming standard 8-hour workday:

OE = DHTW 480

CE = CTWA,N[0,TW] OE

Steady-State Mixing Factor Model

Equations specific to the steady-state mixing fac- tor model are provided below.

VC generation rate:

Gw,day = MEWH EWCF2

Gcw,day = Gw,day NCW

Time-weighted average concentration:

CTWA,N[0,TW] = FC Gw, day

k + Gcw,day

Q · Tw · CF1

CTWA,F[0,TW] = FC Gw,day + Gcw,day

Q · Tw · CF1

Steady-State Three-Zone Model

Equations specific to the steady-state three-zone model are provided below.

Compartments: Zone 0: Outside Zone 1: Near field Zone 2: Salon area Zone 3: Rest of home Flow rates (assumes balanced flow between

rooms and negligible outdoor concentration):

VR = VF−VS

Q20 = ARVSCF4

Q30 = ARVRCF4

Q12 = Q21 = β · CF3CF4

Q23 = Q32 = ARTRVSCF4

Mass balance at a steady state:

−C1 Q12 + C2 Q21 + Gw,day = 0

C1 Q12 + C3 Q32 − C2(Q21 + Q23 + Q20) = 0

C2 Q23 − C3(Q32 + Q30) = 0

Multizone Exposure Modeling: Historical Use of Vinyl Chloride in Hairspray 1723

Solve system of equations (e.g., Cramer’s Rule):⎛ ⎜⎜⎜⎝

−Q12 Q12

0

Q21

−(Q21 + Q23 + Q20) Q23

0

Q32

−(Q32 + Q30)

⎞ ⎟⎟⎟⎠

⎛ ⎜⎜⎜⎝

C1

C2

C3

⎞ ⎟⎟⎟⎠

=

⎛ ⎜⎜⎝

−Gw,day 0

0

⎞ ⎟⎟⎠

Time-weighted average concentration: Near field: CTWA,N[0,TW] = FCC1/CF1 Salon: CTWA,F[0,TW] = FCC2/CF1 Rest of home: CTWA,F[0,TW] = FCC3/CF1

REFERENCES

1. Jones JH. Worker exposure to vinyl chloride and poly(vinyl chloride). Environmental Health Perspectives, 1981; 41:129– 136.

2. Kroschwitz JJ, Grant MU. Vinyl Chloride, in Kirk-Othmer Encyclopedia of Chemical Technology. New York: John Wi- ley and Sons, 1991.

3. USATSDR. Toxicological Profile for Vinyl Chloride. At- lanta, GA: U.S. Agency for Toxic Substances and Disease Registry, 1989.

4. ACGIH. Documentation of the Threshold Limit Values (TLVs): Vinyl Chloride. Cincinnati, OH: American Confer- ence of Governmental Industrial Hygienists, 1962.

5. ACGIH. Documentation of the Threshold Limit Values (TLVs): Vinyl Chloride. Cincinnati, OH: American Confer- ence of Governmental Industrial Hygienists, 1966.

6. Patty FA. Industrial Hygiene and Toxicology, Vol. II. New York: Interscience, 1963.

7. Kielhorn J, Melber C, Wahnschaffe U, Aitio A, Mangelsdorf I. Vinyl chloride: Still a cause for concern. Environmental Health Perspectives, 2000; 108(7):579–588.

8. Veltman G, Lange CE, Juhe S, Stein G, Bachner U. Clinical manifestations and course of vinyl chloride disease. Annals of the New York Academy of Sciences, 1975; 246:6–17.

9. Viola PL, Bigotti A, Caputo A. Oncogenic response of rat skin, lungs, and bones to vinyl chloride. Cancer Research, 1971; 31(5):516–522.

10. Creech JL, Johnson MN. Angiosarcoma of liver in the manufacture of polyvinyl chloride. Journal of Occupational Medicine, 1974; 16(3):150–151.

11. Tabershaw IR, Gaffey WR. Mortality study of workers in the manufacture of vinyl chloride and its polymers. Journal of Oc- cupational Medicine, 1974; 16(8):509–518.

12. Falk H, Herbert J, Crowley S, Ishak KG, Thomas LB, Pop- per H, Caldwell GG. Epidemiology of hepatic angiosarcoma in the United States: 1964–1974. Environmental Health Per- spectives, 1981; 41:107–113.

13. Ward E, Boffetta P, Andersen A, Colin D, Comba P, Ded- dens JA, De Santis M, Engholm G, Hagmar L, Langard S, Lundberg I, McElvenny D, Pirastu R, Sali D, Simonato L. Up- date of the follow-up of mortality and cancer incidence among European workers employed in the vinyl chloride industry. Epidemiology, 2001; 12(6):710–718.

14. Reitz RH, Gargas ML, Andersen ME, Provan WM, Green TL. Predicting cancer risk from vinyl chloride exposure with

a physiologically based pharmacokinetic model. Toxicology and Applied Pharmacology, 1996; 137(2):253–267.

15. Zocchetti C. Angiosarcoma of the liver in man: Epidemiolog- ical considerations. Medicina Del Lavoro, 2001; 92:39–53.

16. Baxter PJ, Anthony PP, Macsween RN, Scheuer PJ. An- giosarcoma of the liver: Annual occurrence and aetiology in Great Britain. British Journal of Industrial Medicine, 1980; 37(3):213–221.

17. Brady J, Liberatore F, Harper P, Greenwald P, Burnett W, Davies JN, Bishop M, Polan A, Vianna N. Angiosarcoma of the liver: An epidemiologic survey. Journal of the National Cancer Institute, 1977; 59(5):1383–1385.

18. Simonato L, L’Abbe KA, Andersen A, Belli S, Comba P, Engholm G, Ferro G, Hagmar L, Langard S, Lundberg I, Pirastu R, Thomas P, Winkelmann R, Saracci R. A collabora- tive study of cancer incidence and mortality among vinyl chlo- ride workers. Scandinavian Journal of Work, Environment & Health, 1991; 17(3):159–169.

19. Lee FI, Smith PM, Bennett B, Williams DM. Occupation- ally related angiosarcoma of the liver in the United Kingdom 1972–1994. Gut, 1996; 39(2):312–318.

20. Kono S, Tokudome S, Ikeda M, Yoshimura T, Kuratsune M. Cancer and other causes of death among female beauticians. Journal of the National Cancer Institute, 1983; 70(3):443– 446.

21. Lamba AB, Ward MH, Weeks JL, Dosemeci M. Cancer mor- tality patterns among hairdressers and barbers in 24 US states, 1984 to 1995. Journal of Occupational and Environmental Medicine, 2001; 43(3):250–258.

22. Pukkala E, Nokso-Koivisto P, Roponen P. Changing can- cer risk pattern among Finnish hairdressers. International Archives of Occupational and Environmental Health, 1992; 64(1):39–42.

23. Robinson CF, Walker JT. Cancer mortality among women employed in fast-growing U.S. occupations. American Jour- nal of Industrial Medicine, 1999; 36(1):186–192.

24. Skov T, Lynge E. Cancer risk and exposures to carcinogens in hairdressers. Skin Pharmacology, 1994; 7(1–2):94–100.

25. Kline & Co. Cosmetics and Toiletries: Consumer Industry Analysis. 1969.

26. Kline & Co. Cosmetics and Toiletries: Consumer Industry Analysis. 1972.

27. Hoffman CS. Beauty salon air quality measurements. CTFA Cosmetic Journal, 1973; 5(3).

28. Keil CB (ed). Mathematical Models for Estimating Occupa- tional Exposure to Chemicals. Fairfax, VA: American Indus- trial Hygiene Association Press, 2000.

29. Nicas M, Plisko MJ, Spencer JW. Estimating benzene expo- sure at a solvent parts washer. Journal of Occupation and Environmental Hygiene, 2006; 3(5):284–291.

30. USEPA. Guidelines for Exposure Assessment. Washing- ton, DC: US Environmental Protection Agency, EPA/600Z- 92/001, May 1992.

31. USEPA. Exposure Factors Handbook (Final Report) 1997. Washington, DC: U.S. Environmental Protection Agency, EPA/600/P-95/002F a-c, 1997.

32. ACGIH. Industrial Ventilation: A Manual of Recommended Practice for Design, 26th ed. Cincinnati, OH: American Con- ference of Governmental Industrial Hygienists, 2007.

33. OSHA. Technical Manual. Section 3, Chapter 3. Washing- ton, DC: U.S. Department of Labor, Occupational Safety and Health Administration, 1999.

34. Gaffney S, Moody E, McKinley M, Knutsen J, Madl A, Paustenbach D. Worker exposure to methanol vapors during cleaning of semiconductor wafers in a manufacturing setting. Journal of Occupational and Environmental Hygiene, 2008; 5(5):313–324.

35. Cherrie JW. The effect of room size and general ven- tilation on the relationship between near and far-field

1724 Sahmel et al.

concentrations. Applied Occupational and Environmental Hygiene, 1999; 14(8):539–546.

36. Pitcher JM. Background Analysis of Vinyl Chloride Usage. Washington, DC: U.S. Consumer Product Safety Commis- sion, 1974.

37. US Senate. Hearing before the Subcommittee on Environ- ment of the Committee on Commerce United States Senate Ninety-Third Congress Second Session on Dangers of Vinyl Chloride. Transcript, Serial Number 93-110, 1974.

38. Estrin NF. Vinyl Chloride. The CTFA Scientific Advisory Committee, 1974.

39. Aviado DM. Toxicity of propellants, in Proceedings of the 4th Annual Conference on Environmental Toxicology, Aerospace Medical Research Laboratory. Wright-Patterson Air Force Base, Ohio, 1973.

40. Bridbord K, Brubaker PE, Gay B, Jr., French JG. Exposure to halogenated hydrocarbons in the indoor environment. En- vironmental Health Perspectives, 1975; 11:215–220.

41. Johnsen MA. The Aerosol Handbook. 1972: 269–271. 42. Bennet H. The Chemical Formulary. Vol. XII. New York:

Chemical Publishing Company, 1965. 43. Bennet H. The Chemical Formulary. Vol. XIII. New York:

Chemical Publishing Company, 1967. 44. Aerosol age survey shows: Opinions vary on what fields are

most promising for greatest growth—But 65% believe that 100% expansion or more will take place in next five years (unauthored). Aerosol Age, 1956; 1(1):28–29.

45. Downing RC, Madinabeitia D. The toxicity of fluorinated hy- drocarbon aerosol propellants. Aerosol Age, 1960; 5:25–27, 74–75.

46. Draize JH, Nelson AA, Newburger SH, Kelly EA. Aerosol hairsprays—FDA reports on extensive studies which demon- strated safety to consumers. Aerosol Age, 1959; 4:36–39, 70– 75.

47. Gunn-Smith RA, Platt NE. Examining aerosol spray patterns. Aerosol Age, 1961; 6:33–34.

48. Herzka A. Spray patterns for aerosol cosmetics. Aerosol Age, 1961; 6:20–22, 70–73.

49. Lefebvre M, Tregan R. Factors affecting particle size distri- bution of an aerosol spray. Aerosol Age, 1965; 10:31–42.

50. Manufacturing Chemist & Aerosol News (unauthored), 1968; 39(2):71.

51. Manufacturing Chemist & Aerosol News (unauthored), 1969; 40(2):57.

52. Martin JW. How and why shellac is widely used in hairsprays. Aerosol Age, 1966; 11:14–17.

53. Sanders PA. A method for evaluating the spray properties of aerosol products. Aerosol Age, 1966; 11:38–46.

54. Scott RJ. Propellant blends ten years after. Aerosol Age, 1971; 26–28.

55. Sanders PA. An empirical method for evaluating the spray properties of aerosol products. Aerosol Age, 1966; 11:31– 35.

56. Johnsen MA. A primer on propellant blends. Aerosol Age, 1963; 8:29.

57. Clairol Company Documents. 1967–1973. 58. Johnsen MA. Personal interview with ChemRisk, 2003. 59. Labreche F, Forest J, Trottier M, Lalonde M, Simard R. Char-

acterization of chemical exposures in hairdressing salons. Applied Occupational and Environmental Hygiene, 2003; 18(12):1014–1021.

60. van Muiswinkel WJ, Kromhout H, Onos T, Kersemaekers W. Monitoring and modelling of exposure to ethanol in hairdressing salons. Annals of Occupational Hygiene, 1997; 41(2):235–247.

61. ASHRAE. Guide and Data Book. Atlanta, GA: American Society of Heating Refrigerating and Air Conditioning Engi- neers, 1964.

62. ASHRAE. Standards for Natural and Mechanical Ventila-

tion. Atlanta, GA: American Society of Heating Refrigerat- ing and Air Conditioning Engineers, 1973.

63. Meikleham RS. On the History and Art of Warming and Ven- tilating Rooms and Buildings. London: George Bell, Fleet Street, 1845.

64. Yaglou CP, Riley EC, Coggins DI. Ventilation requirements. Transactions (ASHVE), 1936; 42(1031):133–162.

65. Klauss AK, Tull RH, Roots LM, Pfafflin JR. History of the changing concepts in ventilation requirements. ASHRAE Journal, 1970; 51–55.

66. Cain WS, Leaderer BP, Isseroff R, Berglund LG, Huey RJ, Lipsitt ED, Perlman LG. Ventilation requirements in buildings—I. Control of occupancy odor and tobacco smoke odor. Atmospheric Environment, 1983; 17(6):1183–1197.

67. Berg-Munch B, Clausen G, Fanger PO. Ventilation require- ments for the control of body odor in spaces occupied by women. Environment International, 1986; 12:195–199.

68. Bremmer HJ, Prud’homme de Lodder LCH, van Engelen JGM. Cosmetics Fact Sheet: To Assess the Risks for the Consumer. Updated Version for ConsExpo 4. The Nether- lands: Centre for Substances and Integrated Risk Assessment (RIVM), 2006; 23–26.

69. Baldwin PE, Maynard AD. A survey of wind speeds in indoor workplaces. Annals of Occupational Hygiene, 1998; 42(5): 303–313.

70. Leino T, Kahkonen E, Saarinen L, Henriks-Eckerman ML, Paakkulainen H. Working conditions and health in hairdress- ing salons. Applied Occupational and Environmental Hy- giene., 1999; 14(1):26–33.

71. Nazaroff WW, Doyle, SM, Nero AV, Sextro RG. Radon entry via potable water. In Nazaroff WW, Nero AV (eds). Radon and Its Decay Products in Indoor Air. New York: John Wiley and Sons, 1988.

72. USEPA. RISK Model, 2007. Available at: http://www.epa. gov/appcdwww/iemb/risk.htm, Accessed on January 2007.

73. ACGIH. Documentation of the Threshold Limit Values (TLVs): Vinyl Chloride. Cincinnati, OH: American Confer- ence of Governmental Industrial Hygienists, 2001.

74. Krajewski J, Dobecki M, Gromiec J. Retention of vinyl chlo- ride in the human lung. British Journal of Industrial Medicine, 1980; 37(4):373–374.

75. Hollund BE, Moen BE. Chemical exposure in hairdresser sa- lons: Effect of local exhaust ventilation. Annals of Occupa- tional Hygiene, 1998; 42(4):277–282.

76. Gay BW, Lonneman WA, Bridbord K, Moran JB. Measure- ments of vinyl chloride from aerosol sprays. Annals of the New York Academy of Science, 1975; 246:286–295.

77. Delmaar JE, Park MVDZ, Engelen JGMV. ConsExpo 4.0, Consumer Exposure and Uptake Models Program Manual. The Netherlands: Centre for Substances and Integrated Risk Assessment (RIVM), 2006.

78. Kuebler H. Vinyl chloride and methylene chloride. P. & E.O.R, 1961; 238–241.

79. Armstrong TW, Haas CN. Quantitative microbial risk assessment model for Legionnaires’ disease: Assessment of human exposures for selected spa outbreaks. Journal of Occupational and Environmental Hygiene, 2007; 4(8): 634–646.

80. Eickmann U, Liesche A, Wegscheider W. Harmonization and further development of models to calculate airborne contam- inant concentrations at the workplace. Expositionsmodell, Gefahrstoffe – Reinhaltung der Luft, 2007 April; 67(4):127– 132.

81. Keil C, Murphy R. An application of exposure modeling in exposure assessments for a university chemistry teaching laboratory. Journal of Occupational and Environmental Hy- giene, 2006; 3(2):99–106.

82. Keil CB. The development and evaluation of an emission fac- tor for a toluene parts-washing process. American Industrial

Multizone Exposure Modeling: Historical Use of Vinyl Chloride in Hairspray 1725

Hygiene Association Journal, 1998; 59:14–19. 83. Keil CB, Nicas M. Predicting room vapor concentrations due

to spills of organic solvents. American Industrial Hygiene As- sociation Journal, 2003; 64(4):445–454.

84. Nicas M. Two Zone Model. In Keil C (ed). Mathematical Models for Estimating Occupational Exposure to Chemicals. Fairfax, VA: American Industrial Hygiene Association Press, 2000.

85. Nicas M. Using mathematical models to estimate exposure to workplace air contaminants. Chemical Health and Safety, 2003b; January/February.

86. Spencer JW, Plisko MJ. A Comparison Study Using a Math- ematical Model and Actual Exposure Monitoring for Esti- mating Solvent Exposures During the Disassembly of Metal Parts. Annapolis, MD: Environmental Profiles, 2007.

87. Vernez D, Bruzzi R, Kupferschmidt H, De-Batz A, Droz P, Lazor R. Acute respiratory syndrome after inhalation of waterproofing sprays: A posteriori exposure-response assess- ment in 102 cases. Journal of Occupational and Environmen- tal Hygiene, 2006; 3(5):250–261.

88. Vernez DS, Droz PO, Lazor-Blanchet C, Jaques S. Characterizing emission and breathing-zone concentrations following exposure cases to fluororesin-based waterproofing

spray mists. Journal of Occupational and Environmental Hy- giene, 2004; 1(9):582–592.

89. Von Grote J, Hurlimann C, Scheringer M, Hungerbuhler K. Reduction of occupational exposure to perchloroethylene and trichloroethylene in metal degreasing over the last 30 years: Influences of technology innovation and legislation. Journal of Exposure Analysis and Environmental Epidemi- ology, 2003; 13:325–340.

90. Von Grote J, Hurlimann C, Scheringer M, Hungerbuhler K. Assessing occupational exposure to perchloroethylene in dry cleaning. Journal of Occupational and Environmental Hy- giene, 2006; 3:606–619.

91. Kersemaekers WM, Verheijen N, Kromhout H, Roeleveld N, Zielhuis GA. Assessment of exposure to solvents among hairdressers: Reliability of a classification scheme and ques- tionnaire. Occupational and Environmental Medicine, 1998; 55(1):37–42.

92. Nicas M. Estimating methyl bromide exposure due to off- gassing from fumigated commodities. Applied Occupational and Environmental Hygiene, 2003a; 18(3):200–210.

93. Keil CB. A tiered approach to deterministic models for in- door air exposures. Applied Occupational and Environmen- tal Hygiene, 2000; 15(1):145–151.

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