Benzene workplace exposure

BTX processing has come under steadily increasing pressure to reduce emissions and workplace exposures (see Industrial hygiene). Reductions in the permissible levels of both benzene and total aromatics (BTX) in gasoline have been legislated. Whereas all BTX components ate to be controUed, the main focus is on benzene because it is considerably mote toxic than the others and is classified as a known carcinogen (42). 

Workplace exposure limits for benzene have been regulated to levels as low as 0.5 ppm (43). Industrial emissions affecting the pubHc ate now low enough that the EPA considers that a greater hazard exists from mosdy indoor sources such as smoking, automobile exhausts, and consumer products (44). 

Money CD, Gray CN. 1989. Exhaled breath analysis as a measure of workplace exposure to benzene ppm. Ann Occup Hyg 33 257-262. 

The effect of this new policy will be the development, whenever possible, of quantitative RELs that are based on human and/or animal data, as well as on the consideration of technological feasibility for controlling workplace exposures to the REL. Under the old policy, RELs for most carcinogens were non-quantitative values labeled lowest feasible concentration (LFC). [Note There are a few exceptions to LFC RELs for carcinogens (e.g., RELs for asbestos, formaldehyde, benzene, and ethylene oxide are quantitative values based primarily on analjdical limits of detection or technological feasibility). Also, in 1989, NIOSH adopted several quantitative RELs for carcinogens from OSHA s permissible exposure limit (PEL) update.]... 

Chronic Health Effect A chronic health effect is an adverse health effect resulting from long-term exposure to a substance. The effects could be a skin rash, bronchitis, cancer, or any other medical condition. An example would be liver cancer from inhaling low levels of benzene at your workplace over several years. The term is also applied to a persistent (months, years, or permanent) adverse health effect resulting from a short-term (acute) exposure. Chronic effects from long-term exposure to chemicals are fairly common. Recognize the PEL (permissible exposure level) for each substance in your workplace and minimize your exposure whenever possible. 

Many very hazardous solvents, such as benzene and carbon tetrachloride, were widely used until the 1970s. The situation was very similar for the use of pesticides. Among the toxic pesticides that were still in wide use 20 years ago were chlorophenols, DDT, lindane, and arsenic salts, all of which are classified as human carcinogens as well as being acutely toxic. Fortunately, use of these kinds of very toxic chemicals is now limited in the industrialized world. However, because the number of chemicals used in various industries continues to increase, the risks of long-term health hazards due to long-term exposure to low concentrations of chemicals continues to be a problem in the workplace. 

Regarding styrene, the variety of controlled human oral and inhalation studies that relate dose to urinary concentration and the existence of a pharmacokinetic model (Droz and Guillemin 1983) could facilitate interpretation of mandelic acid concentration in urine. A caveat in this regard is that other chemical exposures can produce mandelic acid in urine, such as ethyl benzene, acetophenone, and phenylglycine (ACGIH 1991). Those background sources would be more likely to confound low-level general-population biomarker results than workplace end-of-shift results. 

After exposure to benzene, several factors determine whether harmful health effects will occur and if they do, what the type and severity of these health effects might be. These factors include the amount of benzene to which you are exposed and the length of time of the exposure. Most data involving effects of long-term exposure to benzene are from studies of workers employed in industries that make or use benzene. These workers were exposed to levels of benzene in air far greater than the levels normally encountered by the general population. Current levels of benzene in workplace air are much lower than in the past. Because of this reduction, and the availability of protective equipment such as respirators, fewer workers have symptoms of benzene poisoning. 

Two studies of workers exposed to low levels of benzene in the workplace showed slight decreases in erythrocyte counts. A morbidity study of 282 workers in a chemical factory reported that 10 persons who were exposed to over 25 ppm of benzene in the workplace for an average of 9 years (range 3-29 years) had an increased mean corpuscular volume at the end of the high exposure period (1963), but normal values 11 years later (1974) (Fishbeck et al. 1978). Further study of these 282 workers revealed slight decreases in erythrocyte counts that were not correlated with levels of benzene exposure (2-35 ppm) or with duration of employment (1 month to over 20 years) (Townsend et al. 1978). 

The clinical and epidemiological evidence is summarized below. The deficiencies in the studies include the lack of appropriate sampling techniques, exposure determinations, mortality standards, and other aspects of experimental design or methodology. Additionally, intermittent exposures to benzene made it difficult to assume that the average concentrations of benzene measured in a workplace actually indicated the true exposure experienced by each worker (Goldstein 1985). A cause-effect relationship between benzene and leukemia is sufficiently clear however, there are few data from which dose-response relationships can be established. 

Studies of occupational exposure to benzene suggest that absorption occurs both by inhalation and dermally in many workplace settings. In a study conducted in 1992 in Finland, car mechanics exposure to benzene was evaluated (Laitinen et al. 1994). Different workphases were measured at 5 Finnish garages. Blood samples from car mechanics (8 nonsmokers) were taken 3-9 hours after exposure to... 

Chronic-Duration Exposure and Cancer. The primary target for adverse systemic effects of benzene following chronic exposure is the hematological system. Hematological toxicity was reported in studies of humans chronically exposed to benzene in the air in the workplace (Aksoy and Erdem 1978 Aksoy et al. 1971, 1972, 1974, 1987 Cody et al. 1993 Doskin 1971 Erf and Rhoads 1939 Goldwater 1941 Greenburg et al. 1939 Kipen et al. 1989 Li et al. 1994 Townsend et al. 1978 Yin et al. 1987c). 

Individuals employed in industries that use or make benzene or products containing benzene may be exposed to the highest concentrations of benzene. The National Occupational Exposure Survey (NOES), conducted by NIOSH from 1981 to 1983, estimated that approximately 272,300 workers employed in various professions were potentially exposed to benzene in the United States. Approximately half of these workers were employed in general medical and surgical hospitals, and their occupations included nurses and aides, physicians, technicians, technologists, therapists, dieticians, pharmacists, and janitors (NIOSH 1989). The NOES database does not contain information on the frequency, concentration, or duration of exposure the survey provides only estimates of workers potentially exposed to chemicals in the workplace. The current OSHA permissible limit for an 8-hour TWA exposure to benzene is 1 ppm and a... 

OSHA requires employers of workers who are occupationally exposed to benzene to institute engineering controls and work practices to reduce and maintain employee exposure at or below permissible exposure limits (PEL). If the employer can document that benzene is used in the workplace less than 30 days per year, the employer can use any combination of engineering controls, work practice controls, or respirators to reduce employee exposure to or below the (PEL) of 1 ppm. However, the employer must use... 

Exposure limits The U.S. EPA has set the maximum permissible level of benzene in drinking water at 5 ppb of water. OSHA has set limits of 1 ppm of workplace air for 8 hours (TWA). NIOSH recommends that the benzene be treated as a potential human carcinogen and that the exposure limit be regulated as a potential human carcinogen. ... 

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