Chemical Manufacturers, Workers and Chloroprene Vapor Exposure
What health effects are associated with chloroprene vapor exposure?
- By Bernard Fontaine
- Mar 06, 2023
The U.S. Department of Justice is seeking to compel a chemical manufacturing plant to curb its environmental emissions in a region where the estimated cancer risk is among the highest in the U.S. The action raises the stakes in a longstanding conflict between the Louisiana plant, nearby residents and the U.S. Environmental Protection Agency (EPA). The lawsuit alleges emissions at the Pontchartrain Works facility (subsidiary of the U.S. chemical giant DuPont) which constructed the plant in LaPlace, LA, violated the Clean Air Act and “presents an imminent and substantial endangerment to public health and welfare.”
The current Japanese company Denka Performance Elastomer (DPE) is the only facility in the U.S. that still produces chloroprene (2-chloro-1,3-butadiene; β-chlorobutadiene), a chemical used to produce neoprene. Neoprene is a synthetic rubber found in many different commercial products such as s including adhesives, automotive and industrial parts (e.g., belts and hoses), wire and cable covers, caulks, flame-resistant cushioning and other applications requiring chemical, oil and/or weather resistance. The Denka facility has been on the EPA’s radar for years after a 2011 National Air Toxics Assessment revealed: “estimated higher than expected levels of chloroprene in the community of LaPlace, LA.” In 2018, DPE published a statement that new emissions control technology reduced emissions at the plant. This was one of four main DPE projects performed at a cost of nearly $30 million.
In 2014, DuPont was cited by OSHA under 29 CFR 1910.119 Process Safety Management (PSM) of highly hazardous chemicals but no referral was issued for an industrial hygiene evaluation. DuPont was also cited for inadequate medical services and first aid. In 2017, OSHA conducted a safety inspection when a worker fell through a floor grate while observing a recovery column and subsequently was hospitalized. A serious citation was issued to DPE for inadequate walking-working surfaces. Another referral in 2022 resulted in no citations.
DuPont sold the neoprene polychloroprene business to DPE in 2015, after the EPA’s decision to classify chloroprene as a likely human carcinogen in 2010. DuPont remains the landowner of the Denka’s facility and acts as a landlord, according to the complaint. DuPont may need to grant permissions in order for emissions to be reduced. Chloroprene occurs as a colorless, mobile, flammable and volatile liquid that is slightly soluble in water. The vapor pressure for chloroprene is 188 mm Hg at 20 degrees Celsius, which may a relatively volatile organic solvent.
Even when Denka's facility was shut down for a month in September 2021 after Hurricane Ida, monitoring by the Louisiana State University School of Public Health revealed detectable levels of chloroprene in two out of 10 ambient air samples, according to the researchers. That 2021 test, which was not a formal study, found levels approximately four times above the EPA’s recommended maximum annual average chloroprene concentration. EPA air monitoring around the facility has consistently shown readings well in excess of the recommended lifetime exposure limit of 0.2 micrograms per cubic meter (µg/m3).
LaPlace is in the majority-Black St. John the Baptist Parish, about 30 miles outside of New Orleans. The plant is one of many that activists argue puts undue health risks on Black communities in the area. The company said that it "remains committed to identifying and implementing additional emission reductions where possible." The Denka facility is along a stretch of the Mississippi River that activists and residents have nicknamed "Cancer Alley" because of the unusually high cancer risk among communities there and the emissions that come from the numerous plants in the area.
In a letter to Mr. Edward J. Baier, Acting Director, NIOSH, dated December 16, 1974, Dr. John Zapp, Director, Haskell Laboratory, E.I. DuPont de Nemours and Company (DuPont), Wilmington, DE, expressed concern over the potential carcinogenicity of chloroprene (2-chlorobutadiene). DuPont had begun looking closely at this substance recently because of the similarity in chemical structure with vinyl chloride. DuPont has utilized chloroprene in the production of neoprene (polychloroprene) since 1931. Chloroprene is a chemical intermediate largely used as a monomer to manufacture synthetic rubber. It is a chlorine-substituted derivative of 1,3-butadiene, which is a highly OSHA-regulated carcinogen (29 CFR 1910.1051). Vinyl chloride is also a highly regulated chemical substance by OSHA under 29 CFR 1910.1017.
Historical information regarding the adverse health effects of chloroprene exposure was found in the NIOSH Criteria for Recommended Standard (1977). Chloroprene was first synthesized in 1930 by Carothers et al. The first study of chloroprene toxicity was reported by Von Oettingen et al thereafter in 1936. In 1942, Roubal reported an investigation of the toxicologic and hygienic aspects of the Czechoslovak chloroprene rubber industry. This is believed to be the first report of human exposure. Workers involved in the washing and polymerization operations experienced a loss of hair. Other workers complained of a sensation of pressure in the chest with a rapid pulse, severe fatigue and conjunctivitis and necrosis of the corneal epithelium. Albumin was reported to be present in the urine of a small number of workers who, according to Roubal, presumably had had massive chloroprene exposure.
Nystrom described a series of medical studies carried out in Swedish chloroprene plants between 1944 and 1947. These were the first and only studies to include experimental reports of human exposure to airborne chloroprene and to report a human fatality. Experimental exposure of human subjects to chloroprene at 973 parts per million (ppm) led to nausea and giddiness in 15 minutes in resting subjects and in five to 10 minutes in subjects performing light work. Nystrom noted anemia in pilot plant workers who were exposed to air concentrations estimated to be approximately 459 ppm. The range of concentrations of chloroprene in the air was from 56 to greater than 334 ppm in the main chloroprene plant after the full operation was achieved. According to NIOSH, airborne exposures above 300 ppm are considered Immediately Dangerous to Life and Health.
Workers, especially those in the fractional distillation department, developed extreme fatigue and unbearable chest pains after exertion about one month after starting work. The symptoms were particularly severe by the end of the workday. Because of fatigue and severe chest pains, 90 percent of the workers often had great difficulty bicycling to their homes after work and had to rest repeatedly. Both pain and fatigue usually subsided by the following morning, returning during the next workday. Workers also noted changes in their personalities towards irritability and quick-tempered behavior. Contact dermatitis (25 to 30 percent) and reversible hair loss were also noted in some workers, especially in the polymerization area, where 90 percent of the workers showed hair loss.
According to the 1981–83 National Occupational Exposure Survey (NOES, 1997), as many as 18,000 workers in the United States were potentially exposed to chloroprene vapor. National estimates of workers potentially exposed were not available from other countries. Occupational exposures to chloroprene have been measured mainly in polymer production. During 1973, at a chloroprene polymerization plant in the U.S., airborne concentrations of chloroprene were found to range from 14 to 1420 ppm (50 to 5140 mg/m3) in the make-up area, from 130 to 6760 ppm (470 to 24,470 mg/m3) in the reactor area, from 6 to 440 ppm (22 to 1660 mg/m3) in the monomer recovery area and from 113 to 252 ppm [409 to912 mg/m3] in the latex area (Infante et al., 1977). Concentrations in the air inside a Russian polychloroprene rubber plant were 4.0 to 14.8 ppm (14.5 to 53.4 mg/m3) [Mnatsakayan et al., 1972]. In a Russian chloroprene latex manufacturing facility, airborne chloroprene concentrations varied from 0.3 to 2.2 ppm (1 to 8 mg/m3) (Volkova et al., 1976).
Recent data from two chloroprene polymerization plants in the U.S. with 650 to 800 exposed workers show relatively little decline in average exposure concentrations from the late 1970s through 1996. This is partly due to the fact that workers with jobs having a low potential for exposure are no longer routinely monitored, resulting in upwardly biased Time-Weighted Average (TWA) exposure. At present, however, the average exposure of process operators and mechanics is typically below 5 ppm, while other workers in these facilities are exposed to concentrations below 2 ppm (DuPont Dow Elastomers, 1997). Exposure to residual chloroprene monomer in polychloroprene latex and polymer has been described. In 1977, mean airborne concentrations of chloroprene of up to 0.2 ppm (0.72 mg/m3) were reported in a roll-building area at a metal fabricating plant in the U.S. where polychloroprene was applied extensively to metal cylinders before vulcanization (Infante, 1977). Workers in a Russian shoe factory were reportedly often exposed to chloroprene concentrations of 5.5 to 6.9 ppm (20 to 25 mg/m3) [Buyanov and Svishchev, 1973].
Chloroprene has been manufactured at the DPE site since 1969, thus it constitutes a chronic (more than five decades) worker exposure. Based on air monitoring data from both EPA and Denka, chloroprene continues to occur with some regularity at levels exceeding 0.2 µg/m3, even after emission control technologies were installed in February 2018. In 2021, chloroprene air concentrations were as high as 1.8 µg/m3 at a site two miles away from the facility (at Edgard Courthouse, Site #7); and as high as 20.2 µg/m3 at a site one mile from the facility (at Ochsner Hospital). When the proximity of 5th Ward Elementary School is considered (0.3 miles or 500 yards from the Denka facility), it is not unexpected that levels were detected at the school in 2021 as high as 20.7 µg/m3 by DPE (103 times higher than 0.2 µg/m3) and up to 3.34 µg/m3 by EPA (16 times higher than 0.2 µg/m3).
EPA uses mathematical models, based on human and animal studies, to estimate the probability of a person developing cancer from breathing air containing a specified concentration of a chemical. EPA calculated an inhalation unit risk estimate of 3 × 104 (µg/m3)1 for chloroprene based on tumor incidence in multiple organ systems of mice and rats. Taking into account the mode of action conclusion, EPA estimates that if an individual were to continuously breathe air containing chloroprene at an average of 0.002 µg/m3 (2 x 10-6 mg/m3) over an entire lifetime, that person would theoretically have no more than a one-in-a-million increased chance of developing cancer as a direct result of breathing air containing this chemical substance. Similarly, EPA estimates that continuously breathing air containing 0.02 µg/m3 (2 x 10-5 mg/m3) would result in not greater than a one-in-a-hundred thousand increased chance of developing cancer, and air containing 0.2 µg/m3 (2 x 10-4 mg/m3) would result in not greater than a one-in-ten thousand increased chance of developing cancer.
When looking at cancer risk, four occupational epidemiological studies reported statistically significant associations (two- to five-fold increased risk) between chloroprene exposure and liver/biliary passage cancer. A few epidemiological studies reported a non-statistically significant increased risk of lung cancer incidence and mortality associated with chloroprene exposure. An inhalation bioassay by the National Toxicology Program (NTP) showed clear evidence of carcinogenic activity in rats and mice, based on increased incidences of neoplasms of the oral cavity, thyroid gland, lung, kidney, liver, skin, mammary glands and other organs.
In 2010, EPA classified chloroprene as likely to be carcinogenic to humans based on statistically significant and dose-related information from the chronic NTP bioassay showing the early appearance of tumors, development of malignant tumors and the occurrence of multiple tumors within and across animal species; evidence of an association between liver cancer risk and occupational exposure to chloroprene; suggestive evidence of an association between lung cancer risk and occupational exposure; proposed mutagenic action of chloroprene; and structural similarities between chloroprene and the known human carcinogens, butadiene and vinyl chloride. EPA additionally concludes that the weight of evidence supports a mutagenic mode of action for chloroprene carcinogenicity.
In 2007, two authors (Marsh G.M. and Buchanich J.M.) and other colleagues published results of an international historical cohort study of workers who were potentially exposed to chloroprene. The cohort comprised 12,430 workers with some work experience at one of two U.S. industrial sites (Louisville, KY (Plant L, n = 5,507) and Pontchartrain, LA (Plant P, n = 1,357)) or two European sites (Maydown, Northern Ireland (Plant M, n = 4,849) and Grenoble, France (Plant G, n = 717)), with earliest chloroprene production dates ranging from 1942 (Plant L) to 1969 (Plant P). Plants L and M synthesized chloroprene with the acetylene process that produced vinyl chloride (VC) exposures. VC is a known risk factor for angiosarcoma of the liver, hepatocellular carcinoma and other types of cancer. The authors quantitatively estimated historical exposures for individual workers for chloroprene and VC and mortality follow-up was through 2000. The study found no evidence of elevated mortality risks from liver, lung or any other cancer site or any non-cancer causes of death. The Marsh et. al. study is still considered the most comprehensive and methodologically rigorous epidemiologic study of chloroprene-exposed workers to date.
The 2017 mortality update of the U.S. portion of our chloroprene cohort study has many strengths and provides new findings from the most definitive study of the human carcinogenic potential of exposure to chloroprene conducted to date. Updates continue to support the conclusion that the risk of death from all cancers or from the sites of a priori interest (lung and liver cancer) is unrelated to exposure to chloroprene or VC at levels experienced by workers in the two U.S. sites. The post hoc elevated risk for breast cancer was confined to Plant L and does not appear to be associated with workplace factors. Additional evaluations of the chloroprene cohort may help explain the differential mortality risk estimates based on internal and external mortality comparisons.
Looking at current occupational health exposures, federal OSHA established a maximum ceiling value of 25 ppm for acute exposures that should never be exceeded during work. NIOSH Recommended Exposure Limit (REL) and the American Conference of Governmental Industrial Hygienists (ACGIH) established a 1 ppm exposure guideline for an 8-hour TWA for more chronic exposure. Exposure to chloroprene occurs by inhalation of the vapor. Workers may be occupationally exposed to chloroprene by both inhalation and/or dermal exposure. Skin notations have been assigned to the use of chloroprene by NIOSH and ACGIH from claims of loss of hair on exposed body parts.
Both NIOSH and ACGIH consider chloroprene exposure as a suspect lung carcinogen in humans and liver and lung cancer in animals. It also can cause upper respiratory tract and eye irritation. Reports of other chronic effects such as liver cancer, reproductive hazards that may cause damage to the developing fetus, spontaneous abortions or interference with sperm production have not been fully investigated. Residents may be exposed to environmental exposures that may occur during its manufacture, transport, and chemical storage. Very little air sampling information was collected by OSHA for manufacturing facilities using or exposing workers to chloroprene.
Of the total 136 air samples collected between 1984 and 2021, only four air samples resulting in worker exposure were reported in Texas and Ohio above non-detectable levels. All four air sample results were slightly below the 1 ppm NIOSH REL and ACGIH TLV, but no air samples were collected to evaluate a ceiling airborne concentration. The chloroprene at the Ohio plant was used to make plastic resins and petrochemicals while the Texas plant produced a variety of industrial organic chemicals. Besides manufacturing chloroprene to make neoprene, there are occupational health exposures in other chemical industries that go under the radar without conducting a proper exposure risk assessment.
EPA reported symptoms from acute (short-term) human exposure to high concentrations of chloroprene include giddiness, headache, irritability, dizziness, insomnia, fatigue, respiratory irritation, nausea, gastrointestinal disorders, dermatitis, temporary hair loss, conjunctivitis and corneal necrosis. Effects on the cardiovascular system (rapid heartbeat, reduced blood pressure) and changes in blood cell parameters (red blood cells, hemoglobin content, white blood cells and platelets) have also been reported in occupationally exposed workers.
Human symptoms from chronic (long-term) exposure in workers are fatigue, chest pains, giddiness, irritability, dermatitis and hair loss. Chronic occupational exposure to chloroprene vapor may contribute to liver function abnormalities, disorders of the cardiovascular system and depression of the immune system. Occupational studies have found that exposure to chloroprene increases the risk of liver cancer. The International Agency for Research on Cancer, NIOSH, National Toxicology Program, the Federal Republic of Germany Maximum and EPA have classified chloroprene as likely to be carcinogenic to humans.
In animals, toxicity in multiple organ systems, including in the respiratory tract, kidney, liver, spleen and forestomach, has been reported in chronic inhalation studies. The EPA Reference Concentration (RfC) for chloroprene is 0.02 milligrams per cubic meter (mg/m3). The RfC is an estimate (with uncertainty spanning perhaps an order of magnitude) of continuous inhalation exposure to the human population (including sensitive subgroups) that is likely to be without appreciable risk of deleterious noncancer effects during a lifetime. It is not a direct estimator of risk but rather a reference point to gauge the potential effects. At exposures increasingly greater than the RfC, the potential for adverse health effects increases. Lifetime exposure above the RfC does not imply that an adverse health effect would necessarily occur. The RfC for chloroprene was identified based on consideration of sensitive cellular effects observed in the nose, lung and blood of male and female rats and female mice, respectively.
Regarding reproductive hazards, a study reported functional disturbances in spermatogenesis in workers exposed to chloroprene and increased spontaneous abortions in the wives of exposed workers. However, insufficient details are available in the reports to adequately evaluate the results. Reproductive effects, including a decreased number of spermatogonia, a decline in sperm motility, an increased number of dead sperm and degeneration of the testes, have been observed in male rats exposed by inhalation or dermal contact. Increased embryonic mortality and decreased fetal weight were reported in rats exposed by inhalation, although contamination may have occurred during this study. No effects on embryonic or fetal survival nor incidence of soft tissue or skeletal defects were observed in other studies of rats exposed by inhalation.
While there are a limited number of exposed workers and types of industries, more emphasis should be given to conducting exposure risk assessments. As indicated, exposure to chloroprene vapor can cause many different acute and chronic health effects including cancer as referenced by the epidemiological studies to date. OSHA process safety inspectors should consider referring chloroprene exposure potential to industrial hygiene staff to evaluate. More emphasis should be given to highly hazardous chemicals so that the chemical industry and other allied stakeholders take appropriate precautions with appropriate engineering and administrative controls to reduce the risk of exposure to workers, the public and the environment.