Chlorhexidine (SED-14, 764; SEDA-23, 247; SEDA-24, 270; SEDA-25, 276)

Immunologic Chlorhexidine allergy has been well described for over 30 years. Hypersensitivity reactions have been considered to be rare, as chlorhexidine is the standard skin disinfectant used before surgery or invasive procedures and is used in the general population in mouthwashes or for disinfection of minor wounds.

Anaphylactic reactions have been reported in surgical patients (SED-14, 764; SEDA-23, 247). Anaphylaxis has been described in four surgical patients after the use of chlorhexidine as a skin disinfectant. All four had a history of minor symptoms, such as rashes or faints, in connection with previous surgery or invasive procedures (1A).

Chlorhexidine allergy has been well described as a result of application to mucous membranes before instrumentation, (SED-14, 764, SEDA-23, 247; SEDA-24, 270). Severe anaphylactic shock after transurethrally applied chlorhexidine gel continues to be reported (2A).

The risk of hypersensitivity with chlor-hexidine-impregnated central venous catheters has not been fully defined. Randomized studies have failed to show an association (SED-24, 270; SEDA-25, 276); however, there have been reports of anaphylaxis after insertion of these catheters (SEDA-22, 262; SEDA-23, 248) and two life-threatening episodes of anaphylaxis in the same patient were attributed to a central venous catheter that had been impregnated with chlorhexidine and sulfadiazine (3A).

Local hypersensitivity reactions to chlor-hexidine-impregnated patches in neonates are known to occur (SEDA-23, 248). A randomized comparison of povidone-iodine and a chlorhex-idine gluconate impregnated dressing for the prevention of central venous catheter infections in neonates showed that the risk of local contact dermatitis limited the use of the chlorhexidine dressing (4c).

Ethylene oxide (SED-14, 761; SEDA-23, 248; SEDA-24, 271; SEDA-25, 277)

Mutagenicity There is limited epidemiolog-ical evidence for an increased risk of cancer among workers exposed to ethylene oxide and it is classified as a human carcinogen based on supporting mechanistic data (SEDA-24, 271).

Ethylene oxide is a genotoxic carcinogen, so the genotype of an individual could determine susceptibility to its mutagenic effects. The effects of glutathione-S-transferase T1 and M1 genotypes on hemoglobin adducts in erythro-cytes and sister chromatid exchange in lymphocytes have been examined in 58 hospital operators of sterilizers that used ethylene oxide and non-exposed workers (5E). The results suggested that the glutathione-S-transferase T1 null genotype was associated with increased formation of ethylene oxide-hemoglobin adducts in relation to occupational exposure. This suggests that individuals with the glutathione-S-transferase T1 null genotype may be more susceptible to the genotoxic effects of ethylene oxide.


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