1-3 butadiene is produced through the processing of petroleum and is mainly used in the production of synthetic rubber, but is also found in smaller amounts in plastics and fuel. Exposure to 1-3 butadiene mainly occurs in the workplace, including the following industries: synthetic elastomer (rubber and latex) production, petroleum refining, secondary lead smelting, water treatment, agricultural fungicides, production of raw material for nylon, and the use of fossil fuels. Exposure can also occur from automobile exhaust; polluted air and water near chemical, plastic or rubber facilities; cigarette smoke; and ingestion of foods that are contaminated from plastic or rubber containers.
1-3 butadiene is often referred to simply as butadiene. However, the general term butadiene includes both the common industrial chemical 1-3 butadiene and 1-2 butadiene, a contaminant in some industrial processes. Physical characteristics of 1-3 butadiene are shown below.
The health effects caused by exposure to 1-3 butadiene can be split into two categories: acute and chronic. Acute exposures can further be split into low and high doses. Acute low exposures may cause irritation to the eyes, throat, nose, and lungs. Frostbite may also occur with skin exposure. Acute high exposures may cause damage to the central nervous system or cause symptoms such as distorted blurred vision, vertigo, general tiredness, decreased blood pressure, headache, nausea, decreased pulse rate, and fainting. Chronic effects caused by exposure to 1-3 butadiene are controversial. Several human epidemiological studies have shown an increase in cardiovascular diseases and cancer. However, due to the small numbers of cancers and confounding factors such as smoking, and simultaneous exposure to benzene and styrene, a true causal relationship cannot be established. Experiments involving chronic exposures to mice and rats have shown a strong causal relationship between 1-3 butadiene exposure and cancer. Animal studies have also shown reproductive and developmental problems. Based on human and animal studies, the EPA has classified 1-3 butadiene as a known human carcinogen. The American Conference of Governmental Industrial Hygienists (ACGIH) has given 1-3 butadiene a rating of A2, suspected human carcinogen.
There are several ways to reduce exposure to 1-3 butadiene. The preferred approach is to utilize engineering controls such as ventilation and process modification. If these controls are not sufficient other controls may be implemented, including requiring respirator protection where ventilation is not feasible, requiring workers to shower and change into street clothes before leaving the plant, and issuing workers protective eye glasses and splash shields as needed.
Butadiene is a reactive monomer used in the production of synthetic rubber (60%) and plastics. Styrene–butadiene rubber, polybutadiene rubber, adiponitrile, styrene–butadiene latex, acrylonitrile–butadiene–styrene resins, and nitrile rubber are used in the manufacture of tires, nylon products, plastic bottles and food wraps, molded rubber goods, latex adhesives, carpet backing and pads, shoe soles, and medical devices. There are no direct consumer uses of butadiene and unreacted monomer is not expected to be present in polymers and plastics made from butadiene.
1-3 butadiene is an important industrial chemical that is a potent carcinogen in mice and a weak carcinogen in rats. Epidemiology studies have shown that workers in the styrene butadiene rubber (SBR) industry have an increased incidence of leukemia, whereas workers in the monomer industry do not. The presence of a potential confounder in the SBR studies, dimethyldithiocarbamate, may explain this difference. Butdiene is metabolized to three genotoxic epoxides, including epoxybutene, epoxybutane diol, and diepoxide. These differ in mutagenic potency by up to 200-fold, with diepoxide being by far the most mutagenic. Metabolism studies focused on epoxybutene and diepoxide and demonstrated that mice produced about 100 times more diepoxide than epoxybutene. Studies on the molecular dosimetry of DNA adducts demonstrated that the epoxybutane diol is responsible for the major DNA adduct of butadiene, N-7-trihydroxy-butylguanine. These data suggest that the epoxybutane diol is formed by the rapid detoxication of the diepoxide by epoxide hydrolase. Epoxide hydrolase is the major pathway for detoxication in humans and rats, whereas glutathione is the major pathway in the mouse. These species differences may result in greater amounts of diepoxide in mice, resulting in much greater genetic insult.