14. Kane MA, Hadler SC, Margolis HS, Maynard JE. Routine prenatal screening for hepatitis B surface antigen. JAMA 1988;259:408-9.

15. Hershow RC, Hadler SC, Kane MA. Adoption of children from countries with endemic hepatitis B: transmission risks and medical issues. Pediatr Infect Dis 1987;6:431-7. 16. Beasley RP, Stevens CE. Vertical transmission of HBV and interruption with globulin. In: Vyas GN, Cohen SN, Schmid R, eds. Viral hepatitis: a contemporary assessment of etiology, epidemiology, pathogenesis and prevention. Philadelphia: Franklin Institute Press, 1978:333-45.

17. Sinatra FR, Shah P, Weissman JY, Thomas DW, Merritt RJ, Tong MJ. Perinatal transmitted acute icteric hepatitis B in infants born to hepatitis B surface antigen-positive and antihepatitis Be-positive carrier mothers. Pediatrics 1982;70:557–9.

18. Delaplane D, Yogev R, Crussi F, Shulman ST. Fatal hepatitis B in early infancy: the importance of identifying HBsAg-positive pregnant women and providing immunoprophylaxis to their newborns. Pediatrics 1983;72:176-80.

19. Immunization Practices Advisory Committee. Recommendations for protection against viral hepatitis. MMWR 1985;34:313-24,329-35.

20. Klontz KC. A program to provide hepatitis B immunoprophylaxis to infants born to HBsAg-positive Asian and Pacific Island women. West J Med 1987;146:195-9.

21. McMahon BJ, Rhoades ER, Heyward WL, et al. A comprehensive programme to reduce the incidence of hepatitis B virus infection and its sequelae in Alaskan Natives. Lancet 1987;2:1134-6.

22. Xu Z-Y, Liu C-B, Francis DP, et al. Prevention of perinatal acquisition of hepatitis B virus carriage using vaccine: preliminary report of a randomized, double-blind placebo-controlled and comparative trial. Pediatrics 1985;76:713-8.

23. Coursaget P, Yvonnet B, Chotard J, et al. Seven-year study of hepatitis B vaccine efficacy in infants from an endemic area (Senegal). Lancet 1986;2:1143-5.

Imported Human Rabies - Australia, 1987

In November 1987, the illness of a 10-year-old Australian boy who had died of acute encephalitis 4 months earlier was confirmed as being rabies. This is the first laboratory-confirmed case of human or animal rabies ever reported from Australia.

The child had traveled with his mother to India, Pakistan, Nepal, Singapore, and Thailand between February and October of 1986, but no animal bites were reported during this period. He remained well until June 23, 1987, when headache developed, followed by fever, vomiting, and chills. During the next few days, he became anorexic, had a few episodes of delirium at night, and had pain in his right arm. Eight days after the onset of illness, incoordination and diplopia developed, along with a progressive weakness in his legs. When admitted to a local hospital, the patient had palsies of the sixth cranial nerve on the right side and of the seventh cranial nerve bilaterally. Analysis of a cerebrospinal fluid specimen showed normal cell counts and normal protein and glucose levels. A diagnosis of atypical Guillain-Barré syndrome versus encephalitis was made, and on the 10th day of illness the patient was transferred to a regional medical center. At that time, he was unable to walk, and his reflexes were decreased on the right side. An electroencephalogram showed slow wave activity consistent with a diffuse encephalitis, and a computerized axial tomography scan was normal. A repeated lumbar puncture on the 12th day of illness showed 50 white blood cells/mm3, 18 red blood cells/mm3, elevated glucose, and normal protein levels. The patient was temporarily intubated because of irregular respiration. On the 14th day of illness, inappropriate antidiuretic hormone secretion, upper airway obstruction, and pneumonia developed, and the left lung collapsed. Seizures began 2 days later. The patient became comatose on the 19th day of illness, and he died 4 days later.

Hospital pathologists found eosinophilic intracytoplasmic inclusions, suggestive of Negri bodies, on fixed sections of brain tissue. A serum sample taken on the 21st day of illness had a rabies neutralizing antibody titer of 1,400 when analyzed at a reference laboratory 4 months later. No specimens were available for virus isolation.

In December, extensive interviews with relatives, friends, and other contacts of the patient revealed that the patient, an animal lover, had been injured by two animals in the 2 years before his death. He was severely scratched by a neighbor's dog 2 months before his onset of illness, but the dog remained healthy and did not have rabies antibodies when tested in December 1987. However, according to a travel companion, the patient was bitten on a finger by a wild monkey at a marketplace in northern India 16 months before the onset of illness. This incident was not reported to the boy's mother. A photograph of the patient feeding the monkeys at this marketplace was found in a school project he had prepared.

Rabies postexposure prophylaxis was recommended for nine health-care workers and four family members and friends who may have been exposed to the patient's saliva or nerve tissue during his illness.

Reported by: K Dunn, BVSc, Commonwealth Dept of Primary Industries and Energy, Barton, Australian Capital Territory. J Faoagali, MBCHB, H Samartunga, MB, Royal Brisbane Hospital, Brisbane; P DeBuse, MB, D Fraser, MB, Royal Children's Hospital, Brisbane; R Stable, MBBS, B Patten, FRACP, D Martin, MBBS, Nambour General Hospital, Nambour; LL Laws, MVSc, Queensland Dept of Primary Industries, Moorooka; T St. George, PhD, Div of Tropical Animal Production, Commonwealth Scientific and Industrial Research Organization, Indooroopilly; RA Ramm, MB, RP Davison, MB, V Kelk, Queensland Dept of Health. Australian Animal Health Laboratory, Commonwealth Scientific and Industrial Research Organization, Geelong, Victoria. Australian Dept of Community Svcs and Health. Viral and Rickettsial Zoonoses Br, Div of Viral Diseases, Center for Infectious Diseases, CDC.

Editorial Note: All available data indicate that this was an imported case of rabies. The only previous report of animal or human rabies in Australia is poorly documented, but, in 1867, a child and a dog from Tasmania had suspected rabies (1). Both animal and human rabies have been reported from all the countries in which the patient traveled except Singapore (2). (Nepal did not contribute to that survey.) The monkey bite in northern India 16 months before the onset of illness must be considered the probable exposure, but the patient might have received other unreported bites while traveling in Asia. If the patient was exposed in Asia, the incubation period would have been between 8 and 16 months. In one large study of human rabies, approximately 1% of cases had incubation periods of over 1 year (3). Cases of monkey-transmitted human rabies are rare; however, one extremely long incubation period (37.5 months) was reported (4).

In the Australian boy's case, paralysis dominated the clinical picture. The clinical picture and the prolonged course before the onset of coma are consistent with the paralytic form of rabies, which occurs in approximately 20% of cases (3).

Since Australia is considered a rabies-free country (2), animal rabies vaccination is not required and animals that bite people are not quarantined. If animal rabies should become endemic in Australia, an estimated 38,000 people per year might have to receive postexposure prophylaxis (5). In addition, millions of dollars would have to be spent on animal rabies vaccination and quarantine. Wild animals that might become reservoirs if rabies should be introduced into Australia include the dingo (a wild dog), red fox, feral cat, and bat. A limited serosurvey of bats in Queensland for rabies antibodies is in progress.

This report emphasizes the importance of rabies preexposure prophylaxis for travelers visiting rabies-endemic countries for more than 30 days (6), especially children who are likely to have unrecognized or unreported exposures. Preexposure prophylaxis can be administered intramuscularly or intradermally (7); however, the intradermal regimen should be completed at least 30 days before departure and should not be used if the person is taking chloroquine for malaria chemoprophylaxis. References

1. Bisseru B. Rabies. London: William Heinemann Medical Books, 1972:18.

2. World Health Organization. World survey of rabies XXII (for years 1984/85). Geneva: World Health Organization, Division of Communicable Diseases, 1987.

3. Hattwick MAW. Human rabies. Public Health Rev 1974;3:229-74.

4. Wilson JM, Hettiarachchi J, Wijesuriya LM. Presenting features and diagnosis of rabies. Lancet 1975;2:1139-40.

5. Nixon J, Pearn J, McGarn F. Dog bite injuries to children: potential rabies threat to Australia. Med J Aust 1980;1:175-6.

6. Centers for Disease Control. Health information for international travel 1987. Washington, DC: US Department of Health and Human Services, Public Health Service, 1987:108-12; DHHS publication no. (CDC)85-8280.

7. Immunization Practices Advisory Committee. Rabies prevention: supplementary statement on the preexposure use of human diploid cell rabies vaccine by the intradermal route. MMWR 1986;35:767-8.

On April 23, 1986, five steam-press operators at an Ohio rubber plant became ill with symptoms including yellow discoloration of the hands, blue discoloration of the lips and nail beds, headache, nausea, chest pain, dizziness, confusion, and difficulty in concentrating. One worker suffered a seizure. Medical examinations showed that blood methemoglobin (MetHb) levels in the workers ranged from 3.8% to 41.2% (normal level <1%).

The workers had been using an adhesive to bond metal studs into rubber strips to be attached to automotive bumpers. When the outbreak occurred, officials of the company voluntarily stopped steam-press operations and asked that representatives from the Occupational Safety and Health Administration (OSHA) and the Ohio Industrial Commission investigate. Five days later, a plant supervisor operated the steam-press for about 2 hours so that an industrial hygienist with the Ohio Industrial Commission could take air samples. After the 2-hour simulation, the supervisor's blood MetHb level was 12.5%. Since the cause of the incident remained unknown 1 week later, plant management requested technical assistance from the National Institute for Occupational Safety and Health (NIOSH) (1).

The product being used is a solvent-borne adhesive that is composed of carbon black (<5% by weight), a proprietary curative system (<5% by weight), and xylene as a solvent (approximately 78% by weight). NIOSH personnel collected bulk samples from the lot ("old" lot) of adhesive used at the time of the outbreak and from a new lot that arrived after the outbreak. Samples were extracted with carbon disulfide and methanol, and the extracts were analyzed by using a gas chromatograph equipped with a flame ionization detector. Para-dinitrobenzene (p-DNB) was identified as a contaminant in the old lot of adhesive. So that concentrations of p-DNB in both the old and new lots could be determined, portions of the samples were extracted and

Methemoglobinemia - Continued

p-DNB standards were dissolved in acetone and analyzed by gas chromatography. The concentration of p-DNB in the old lot (1% by weight) was approximately 30 times that in the new lot (0.03% by weight).

The NIOSH investigation, in conjunction with that of the adhesive manufacturer, revealed that p-DNB had been inadvertently formed during the manufacture of one of the proprietary substances used as a base chemical in the adhesive. This p-DNBcontaminated chemical was then introduced into the adhesive during its formulation. When notified of these findings, the manufacturer of the adhesive recalled all lots thought to be contaminated with significant quantities of p-DNB. The manufacturer also revised the material safety data sheet for this adhesive to indicate that trace amounts of dinitrobenzene, which can cause cyanosis, may be present.

NIOSH recommended that workers in the plant use butyl rubber gloves to avoid skin contact with the dried adhesive and that plant management institute periodic medical monitoring of all workers exposed to the adhesive. After plant officials replaced the p-DNB-contaminated adhesive with another product and implemented the recommendations, the steam-press operations were resumed.

NIOSH personnel monitored workers throughout the first day of operation for any signs of p-DNB exposure. No workers complained of any symptoms during or after the work shift, and none showed evidence of cyanosis during physical examination. To monitor workers for MetHb, NIOSH also collected preshift and postshift blood samples from nine steam-press workers using the new adhesive and from six office workers (controls) with no chemical exposure. MetHb levels in all blood samples were within normal limits and remained essentially unchanged over the workday. Reported by: Hazard Evaluations and Technical Assistance Br; Div of Surveillance, Hazard Evaluations, and Field Studies; National Institute for Occupational Safety and Health, CDC. Editorial Note: Aromatic nitro compounds, such as p-DNB, are used in many industries, including the manufacture of dyes, explosives, pigments, insecticides, textiles, plastics, resins, elastomers, photographic developers, pharmaceuticals, plant-growth regulators, fuel additives, rubber accelerators, and antioxidants (2,3). Because of this wide variety of uses, the potential for occupational exposure to these compounds is great.

The present incident illustrates that excessive exposure to aromatic nitro compounds may cause adverse health effects. p-DNB is readily absorbed by the skin and exerts its adverse health effects via the formation of MetHb from hemoglobin (Hb). Accumulations of MetHb greater than 1% of the total Hb substantially reduce the blood's capacity to carry oxygen to tissues of the body. Symptoms of illness are generally related to the percentage of MetHb in the blood: cyanosis and headache occur first (in persons with greater than 15% MetHb); dizziness and fatigue appear next (with greater than 40% MetHb); and ataxia, shortness of breath, tachycardia, nausea, vomiting, and drowsiness follow and can progress to stupor, coma, and possibly death (when levels exceed 70% MetHb).

The overall effect of substances that form MetHb is known as the "cyanosisanemia syndrome" (4,5). p-DNB ranks second among cyanosis-producing chemicals and is also potent in causing anemia (Table 1).

The current OSHA permissible exposure limit and the American Conference of Governmental Industrial Hygienists (ACGIH) threshold limit value for p-DNB is 1 mg/m3 based on an 8-hour time-weighted average, and the ACGIH notes that p-DNB can be absorbed cutaneously, which can contribute to overall exposure (6). Indeed,

the skin is the main route by which several fat-soluble aromatic nitro compounds, including p-DNB, enter the body. For this reason and also because many nitrobenzene derivatives have low vapor pressures and do not reach high levels in the air, measures of airborne concentrations alone may not be the best indicator of total exposure.

The incident at this plant demonstrates the adverse health effects of a common class of industrial chemicals-aromatic nitro compounds-and emphasizes that employers and employees should know the potential dangers of exposure to these substances as well as to toxic substances in general. Further, since the incident was caused by a contaminated base chemical, the prevention of future episodes also depends on careful quality control in manufacturing that chemical. The actions of company officials in stopping the steam-press operations and cooperating with NIOSH technical personnel led to the rapid and successful resolution of this problem.

TABLE 1. Ranking of 13 chemicals that form methemoglobin and potentially produce cyanosis and anemia*

1. Stephenson RL, Gupta S, Rondinelli R. Health hazard evaluation report no. HETA 86-350-1815. Cincinnati, Ohio: US Department of Health and Human Services, Public Health Service, 1987. 2. Centers for Disease Control, Occupational Safety and Health Administration. NIOSH/OSHA occupational health guidelines for chemical hazards. Cincinnati, Ohio: US Department of Health and Human Services, Public Health Service; US Department of Labor, Occupational Safety and Health Administration, 1981; DHHS publication no. (NIOSH)81-123.

3. International Labour Office. Encyclopaedia of occupational health and safety. Vol 2. 3rd ed. Geneva: International Labour Organization, 1983:1355-6,1451-4.

4. Linch AL, Wuertz RL, Charsha RC. Chemical cyanosis and anemia control. In: Steere NV, ed. CRC handbook of laboratory safety. 2nd ed. West Palm Beach, Florida: CRC Press, 1978:342-78.

5. Linch AL. Biological monitoring for industrial exposure to cyanogenic aromatic nitro and amino compounds. Am Ind Hyg Assoc J 1974;35:426-32.

6. American Conference of Governmental Industrial Hygienists. Threshold limit values and biological exposure indices for 1987-1988. Cincinnati, Ohio: American Conference of Governmental Industrial Hygienists, 1987:20.