Phenol exposure

Brent, R.N. and E.E. Herricks. 1998. Postexposure effects of brief cadmium, zinc, and phenol exposures on freshwater organisms. Environ. Toxicol. Chem. 17 2091-2099. 

Since ETS contains phenol, reducing the amount of smoking indoors will reduce phenol exposures. Household products and over-the-counter medications containing phenol should be stored out of reach of young children to prevent accidental poisonings and skin bums. Always store household chemicals in their original labeled containers. Never store household chemicals in containers that children would find attractive to eat or drink from, such as old soda bottles. Keep your Poison Control Center s number next to the phone. 

Cardiovascular Effects. In a cohort mortality study of workers in a large rubber and tire manufacturing plant, Wilcosky and Tyroler (1983) found a significant increase in mortality from ischemic heart disease in phenol exposed workers. Of the 25 solvents used in the plant, phenol exposure showed the strongest association with mortality from heart disease, greater even than that observed for exposure to carbon disulfide, the only known occupational cause of atherosclerosis. 

An increased susceptibility to Streptococcus zooepidemicus aerosol was not observed in mice exposed to 5 ppm phenol for 3 hours, or for 5 daily 3-hour periods (Aranyi et al. 1986). Neither did the phenol exposures affect pulmonary bactericidal activity towards Klebsiella pneumonia. Although tests for vulnerability to infectious agents do not represent a comprehensive evaluation of immunological competence, the 5-ppm level can be considered a NOAEL for this specific immunological effect, and is recorded in Table 2-1 and plotted in Figure 2-1. 

Phenol is a hydrolyzed metabolite of benzene and is itself further hydrolyzed or conjugated to produce other compounds. Therefore, the toxic effects of phenol exposure may be due to a combination of the parent compound and its metabolites. The major tissues in which metabolism appears to occur are the liver, gut, lung, and kidney (Cassidy and Houston 1984 Powell et al 1974 Quebbemann and Anders 1973 Tremaine et al. 1984). Since phenol, benzene, and their major metabolites all seem to compete for the same P450 and conjugating enzymes, metabolic reactions are presumed to be saturable. 

It has been suggested that phenol exposure results in cardiac effects because it blocks the cardiac sodium channel subtype, with little effect on sodium channels in skeletal muscle (Zamponi et al. 1994). Phenol does not appear to be carcinogenic following oral exposure (NCI 1980), although the chemical combinations that result from benzene and phenol metabolism may contain compounds that do initiate or promote cancer. Metabolites such as hydroquinone and catechol have been demonstrated to be genotoxic and clastogenic. 

Cancer. A small non-significant excess of respiratory cancers among phenol-exposed wood industry workers was not clearly related to phenol exposure (Kauppinen et al. 1986). Although small nonsignificant excesses of Hodgkin s disease and of lung, esophageal, and kidney cancers were noted, mortality from cancer was not clearly related to phenol exposure in phenol production workers (Dosemeci et al. 1991). 

Based on a very limited data set, it is likely that most of the effects of phenol exposure, including cardiac arrhythmias and central nervous system depression, observed in adults will be observed in children if exposures are comparable. The data are insufficient to determine whether children will be especially sensitive to such effects, however. 

Phenol can result in hemolytic anemia. Therefore, red blood cell counts may serve as a useful biomarker of effect following exposure to phenol. Measurement of liver enzymes in the serum following phenol exposure would also be useful to determine if liver effects have occurred. 

The mechanism of action of phenol in the body is not well understood. Reports of cardiac arrhythmias resulting from phenol exposure are not uncommon (Gross 1984 Horch et al. 1994 Truppman and Ellenby 1979 Warner and Harper 1985). Methods to interfere with the mechanism of action for phenol were not identified. 

There was no information found on the placental transfer of phenol or on the concentrations of phenol present in breast milk. There is evidence that benzene and its (not specifically identified) metabolites do cross the placenta, although there is no evidence of selective accumulation (Ghantous and Danielsson 1986). Additional studies of this issue are needed to determine if phenol and its metabolites are among the metabolites of benzene that cross the placenta, and if so whether phenol behaves like benzene in the lack of accumulation. Information is also needed on the content of phenol in breast milk under various conditions, e.g, smoking versus non-smoking mothers, in order to determine if breast milk could ever be a source of phenol exposure for children. 

Some foods containing phenol have been identified (see Section 5.4.4) and could result in low levels of phenol exposure in children. In addition, phenol is produced endogenously as a breakdown product of protein metabolism normal concentrations in urine generally do not exceed 20 mg/L (ACGIH 1991). 

Since phenol can be readily absorbed through the skin (ACGIH 1991), children may be more susceptible to low levels of phenol exposure since they have a higher skin-surface-area to weight ratio. Since young children are more likely to come in contact with the floor and other low-lying areas, they may be exposed to phenol found in consumer products such as general disinfectants used to clean toilets, floors, drains, and other areas (Budavari 1989 CA EPA 1998 Hawley 1981). 

The level of phenol detected in blood or urine may not accurately reflect actual phenol exposure because phenol may also appear as a metabolite of benzene or other drugs. It has been shown that under certain acidic conditions used for the hydrolysis of conjugated phenols, acetyl salicylic acid (aspirin) may produce phenol (Baldwin et al. 1981) and yield spuriously higher values for phenol in blood and urine. 

The changes in metabolite concentrations in human blood, urine, or other appropriate biological media over time may be useful in estimating phenol s rate of metabolism in humans. In some instances, the quantification of metabolites may be useful in correlating the exposure doses to the human body burden. Studies that correlate phenol exposure with levels of metabolites in human biological matrices are not available for this compound, although analytical methods for the quantification of the metabolites are available. 

Pullin TG, Pinkerton MN, Johnson RV, et al. 1978. Decontamination of the skin of swine following phenol exposure A comparison of the relative efficacy of water versus polyethylene glycol/industrial methylated spirits. Toxicol Appl Pharmacol 43 199-206. 

Schmidt R, Maibach H. 1981. Immediate and delayed onset "skip area" dermatitis presumed secondary to topical phenol exposure. Contact Dermatitis 7 199-202. 

Wantke F, Focke M, Hemmer W, et al. 1996. Formaldehyde and phenol exposure during an anatomy dissection course A possible source of IgE-mediated sensitization Allergy 51 837-841. 

In a case-control study of workers in various wood industries, an increased risk for tumors of the mouth and respiratory tract was associated with phenol exposure however, the small number of cases and confounding exposures were inadequately controlled." The lARC has determined that there is inadequate evidence for carcinogenicity of phenol in humans and experimental animals and that it is not classifiable as to its carcinogenicity to humans. ... 

In Siemiatycki s (1991) population-based case-control study of cancer in Montreal, Canada (see monograph on dichloromethane in this volume), phenol was one of the substances evaluated 1% of the entire study population had been exposed to it at some time. Among the main occupations to which phenol exposure was attributed in this study were electric motor repairmen and foundry workers. The publication reported an association between phenol and pancreatic cancer (odds ratio, 4.8 90% CI, 1.8-12.7 n = 4) for no other site was cancer risk associated with phenol exposure. [The Working Group noted that detailed results for other sites were not provided, because they were based on small numbers, and that workers typically had multiple exposures.]... 

Woods, J.S., Polissar. L., Severson, R.K., Heuser, L.S. Kulander. B.G. (1987) Soft tissue sarcoma and non-Hodgkin s lymphoma in relation to phcnoxyherbicide and chlorinated phenol exposure in western Washington. J. natl Cancer Inst., 78. 899-910... 

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