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Therefore, chemoprophylaxis of household or day-care contacts of children with Haemophilus b disease should be directed at vaccinated as well as unvaccinated contacts. Because of the length of time necessary to generate an immunologic response to the vaccines, vaccination does not play a major role in the management of patients with Haemophilus b disease or their contacts. Vaccine may be given to previously unvaccinated children of appropriate age to provide protection against future exposure.

9. Conjugate vaccine and DTP may be given simultaneously at different sites. Data are lacking on concomitant administration of conjugate vaccine and measlesmumps-rubella (MMR) or oral polio (OPV) vaccines. However, if the recipient is unlikely to return for further vaccination, simultaneous administration of all vaccines appropriate to the recipient's age and previous vaccination status is recommended (including DTP, OPV, MMR, and conjugate vaccine).

References

1. Peltola H, Käyhty H, Virtanen M, Mäkelä PH. Prevention of Hemophilus influenzae type b bacteremic infections with the capsular polysaccharide vaccine. N Engl J Med 1984;310: 1561-6.

2. Cochi SL, Broome CV, Hightower AW. Immunization of U.S. children with Hemophilus influenzae type b polysaccharide vaccine: a cost-effectiveness model of strategy assessment. JAMA 1985;253:521-9.

3. Immunization Practices Advisory Committee. Polysaccharide vaccine for prevention of Haemophilus influenzae type b disease. MMWR 1985;34:201-5.

4. Eskola J, Peltola H, Takala AK, et al. Efficacy of Haemophilus influenzae type b polysaccharide-diphtheria toxoid conjugate vaccine in infancy. N Engl J Med 1987;317:

717-22.

5. Lepow ML, Samuelson JS, Gordon LK. Safety and immunogenicity of Haemophilus influenzae type b-polysaccharide diphtheria toxoid conjugate vaccine in infants 9 to 15 months of age. J Pediatr 1985;106:185-9.

6. Käyhty H, Eskola J, Peltola H, Stout MG, Samuelson JS, Gordon LK. Immunogenicity in infants of a vaccine composed of Haemophilus influenzae type b capsular polysaccharide mixed with DPT or conjugated to diphtheria toxoid. J Infect Dis 1987;155:100-6.

7. Berkowitz CD, Ward JI, Meier K, et al. Safety and immunogenicity of Haemophilus influenzae type b polysaccharide and polysaccharide diphtheria toxoid conjugate vaccines in children 15 to 24 months of age. J Pediatr 1987;110:509-14.

8. Berkowitz CD, Ward JI, Hendley JO, et al. Persistence of antibody (AB) to Haemophilus influenzae type b (Hib) and response to PRP and PRP-D booster immunization in children initially immunized with either vaccine at 15 to 24 months [Abstract no. 889]. Pediatr Res 1987;21:321A.

9. Eskola J, Käyhty H, Peltola H, et al. Antibody levels achieved in infants by course of Haemophilus influenzae type b polysaccharide/diphtheria toxoid conjugate vaccine. Lancet 1985;1:1184-6.

10. Lepow ML, Barkin RM, Berkowitz CD, et al. Safety and immunogenicity of Haemophilus influenzae type b polysaccharide-diphtheria toxoid conjugate vaccine (PRP-D) in infants. J Infect Dis 1987;156:591-6.

11. Lepow ML, Randolph M, Cimma R, et al. Persistence of antibody and response to booster dose of Haemophilus influenzae type b polysaccharide diphtheria toxoid conjugate vaccine in infants immunized at 9 to 15 months of age. J Pediatr 1986;108:882-6.

12. Granoff DM, Boies EG, Munson RS. Immunogenicity of Haemophilus influenzae type b polysaccharide-diphtheria toxoid conjugate vaccine in adults. J Pediatr 1984;105:22-7.

13. Frank AL, Labotka RJ, Frisone LR, et al. H. influenza bimmunization of children with sickle cell diseases [Abstract no. 906]. Pediatr Res 1987;21:324A.

14. Cates KL. Serum opsonic activity for Haemophilus influenzae type b in infants immunized with polysaccharide-protein conjugate vaccines. J Infect Dis 1985;152:1076-7.

15. Immunization Practices Advisory Committee. Update: prevention of Haemophilus influenzae type b disease. MMWR 1986;35:170-4,179-80.

Epidemiologic Notes and Reports

PCB Contamination of Ceiling Tiles - Madison, Wisconsin

In November of 1986, a manufacturer of ceiling tiles notified a local public school in Madison, Wisconsin, that the school contained ceiling tiles contaminated with polychlorinated biphenyl (PCB) compounds. The manufacturer offered to replace the tiles, and the Wisconsin Department of Health and Social Services, in cooperation with Madison officials and local representatives of the manufacturer, investigated the potential health hazard. The study included environmental monitoring before and after removal of the contaminated tiles and an analysis of PCB levels in serum samples from the school's staff.

Ceiling tiles manufactured by this company were first identified as a source of PCB contamination of air and surfaces during an investigation of a fire at a community college in New Jersey (1). Following this fire, the company reported that PCBcontaining tiles had been manufactured in limited quantities in 1969 and 1970. The Madison, Wisconsin, public school was one of four sites in the United States known to contain these tiles.

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Before removal of the tiles, air concentrations of PCB (quantified as an isomeric mixture containing 54% chlorine by weight) in the Madison school ranged from 1.6 micrograms per cubic meter (μg/M3) to 5.1 μg/M3 (time-weighted average [TWA] over 17 hours) in areas where ceilings were constructed entirely from the contaminated tiles (mean 2.7 μg/m3). The air in areas with PCB-containing tiles only around the perimeter of the ceiling had intermediate levels of PCBs (mean 1.4 μg/m3, range 1.1 μg/m3 to 1.8 μg/M3). The air in areas without any PCB-containing tiles had lower concentrations of PCBs (mean = 1.0 μg/M3, range 0.9 μg/M3 to 1.0 μg/M3). A total of 17 air samples were analyzed.

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In December 1986, after this initial environmental testing, local officials requested that the manufacturer replace the contaminated tiles as soon as possible. The school's staff and students temporarily moved to a new location in January 1987. Then, using isolation techniques similar to those used in asbestos abatement, the manufacturer removed approximately 30,000 square feet of ceiling tile and cleaned the remaining exposed surfaces. Air monitoring following tile removal showed diminished PCB concentrations. Mean PCB levels in areas where ceilings were constructed entirely from contaminated tiles decreased to 1.1 μg/M3. The mean concentration in areas with PCB-containing tiles only around the perimeter of the ceiling decreased to 1.3 μg/M3. Mean concentration in areas with no PCB-containing tiles decreased to 0.7 μg/M3. New ceiling tiles were then installed, and classes resumed February 17, 1987.

Additional monitoring in May 1987 showed further decreases in air concentrations of PCBs. Areas that had contained only contaminated ceiling tiles had an average concentration of 0.7 μg/M3; areas with contaminated tiles only around the perimeter had an average concentration of 0.8 μg/m3.

The school had been occupied for 16 years, and the average length of employment at that location for the 59 current staff members was 7 years. Serum samples from 73 current and former staff members were biologically monitored to determine whether increased PCB absorption could be detected. When the capillary column method of analysis (2) was used, the geometric mean of all PCB congeners was 1.2 micrograms per liter (μg/L) of blood (range nondetectable to 12.2 μg/L).* In a Finnish

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study using the same laboratory method, the geometric mean for PCB congeners was 1.2±0.6 μg/L for people with no specific exposure to PCBs (2).

Reported by: J Schmidt, PhD, Madison Dept of Public Health; M Rubenstein, PhD, W Sonzogni, PhD, Wisconsin State Laboratory of Hygiene; J Schirmer, MS, H Anderson, MD, Environmental Epidemiologist, Wisconsin Dept of Health and Social Svcs. Div of Field Svcs, Epidemiology Program Office; Div of Environmental Hazards and Health Effects, Center for Environmental Health and Injury Control; Office of the Director, National Institute for Occupational Safety and Health, CDC.

Editorial Note: Although epidemiologic evidence remains inconclusive (3), the International Agency for Research on Cancer has suggested that PCBs be considered "probable" human carcinogens (4), and animal studies indicate a potential for adverse reproductive effects (5-8). For airborne PCBs, the Occupational Safety and Health Administration has promulgated permissible 8-hour TWA exposure limits of 0.5 mg/m3 for PCBs containing 54% chlorine and 1 mg/M3 for PCBs containing 42% chlorine (9). The National Institute for Occupational Safety and Health (NIOSH), CDC, has recommended that occupational exposure by inhalation be limited to an 8-hour TWA ≤1.0 μg total PCBs/M3 (the minimum reliably detectable concentration using the recommended sampling and analytical methods) (10). The initial environmental sampling at the school indicated that PCB concentrations in most working areas exceeded the NIOSH recommended limit. Although PCB air concentrations were lower immediately following removal of the contaminated tiles, they remained above the NIOSH recommended exposure limit. Several months following tile removal, repeat sampling for PCBs documented air concentrations below the NIOSH recommended limit.

The levels of PCBs in serum samples from staff members were similar to levels previously reported in various populations with no known specific exposures to PCBs (11, 12). Environmental data were not available to characterize past exposures in the study population, nor were biological data available to characterize the staff's PCB body burden before exposure to the ceiling tiles. PCB in the serum samples could have been related primarily to accumulation from other sources such as diet (13), with some unknown additional contribution from exposures attributable to the contaminated ceiling tiles. The PCB blood values were well below levels that have been observed in occupational groups that have an increased prevalence of abnormal liver enzymes, one of the subtle effects suggestive of chronic PCB exposure (14). References

1. Centers for Disease Control. PCB contamination of ceiling tiles in public buildings - New Jersey. MMWR 1986;36:89-91.

2. Luotamo M, Järvisalo J, Aitio A. Analysis of polychlorinated biphenyls (PCBs) in human serum. Environ Health Perspect 1985;60:327-32.

3. Brown DP, Jones M. Mortality and industrial hygiene study of workers exposed to polychlorinated biphenyls. Arch Environ Health 1981;36:120-9.

4. International Agency for Research on Cancer. The evaluation of the carcinogenic risk of chemicals to humans: polychlorinated biphenyls and polybrominated biphenyls. Vol. 18. Geneva: World Health Organization, 1978.

5. Villeneuve DC, Grant DL, Khera K, Clegg DJ, Baer H, Phillips WE. Fetotoxicity of a polychlorinated biphenyl mixture (Aroclor 1254) in the rabbit and in the rat. Environ Physiol 1971;1:67-71.

6. Allen JR, Carstens LA, Barsotti DA. Residual effects of short-term, low-level exposure of nonhuman primates to polychlorinated biphenyls. Toxicol Appl Pharmacol 1974;30:440-51. 7. Barsotti DA, Marlar RJ, Allen JR. Reproductive dysfunction in rhesus monkeys exposed to low levels of polychlorinated biphenyls (Aroclor 1248). Food Cosmet Toxicol 1976; 14:99-103.

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8. Allen JR, Barsotti DA. The effects of transplacental and mammary movement of PCBs on infant rhesus monkeys. Toxicol 1976;6:331-40.

9. Centers for Disease Control. NIOSH recommendations for occupational safety and health standards. MMWR 1986;35(suppl 1):27S.

10. National Institute for Occupational Safety and Health. Criteria for a recommended standard: occupational exposure to polychlorinated biphenyls (PCBs). Cincinnati: US Department of Health, Education, and Welfare, Public Health Service, 1977; DHEW publication no. (NIOSH)77-225.

11. Landrigan PJ. General population exposure to environmental concentrations of halogenated biphenyls. In: Kimbrough RD, ed. Halogenated biphenyls, terphenyls, naphthalenes, dibenzodioxins and related products. New York: Elsevier/North-Holland Biomedical Press, 1980:267-86.

12. Wolff MS. Occupational exposure to polychlorinated biphenyls (PCBs). Environ Health Perspect 1985;60:133-8.

13. Kreiss K, Roberts C, Humphrey HEB. Serial PBB levels, PCB levels, and clinical chemistries in Michigan's PBB cohort. Arch Environ Health 1982;37:141-7.

14. Maroni M, Colombi A, Arbosti G, Cantoni S, Foa V. Occupational exposure to polychlorinated biphenyls in electrical workers. Il health effects. Br J Ind Med 1981;38:55-60.

Current Trends

Compendium of Animal Rabies Control, 1988
Prepared by: The National Association

of State Public Health Veterinarians, Inc.*

Part I: Recommendations for Immunization Procedures

The purpose of these recommendations is to provide information on rabies vaccines to practicing veterinarians, public health officials, and others concerned with rabies control. This document will serve as the basis for animal rabies vaccination programs throughout the United States. Its adoption should result in standardization of procedures among jurisdictions, which is necessary for an effective national rabies control program. These recommendations are reviewed and revised as necessary prior to the beginning of each calendar year. All animal rabies vaccines licensed by the U.S. Department of Agriculture and marketed in the United States are listed in Part II of the compendium. Part III describes the principles of rabies control. A. Vaccine Administration

It is recommended that all animal rabies vaccines be restricted to use by or under the supervision of a veterinarian.

B. Vaccine Selection

In comprehensive rabies control programs, it is recommended that only vaccines with a 3-year duration of immunity be used. This practice eliminates the need for annual vaccination and constitutes the most effective method of increasing the proportion of immunized dogs and cats. (See Part II.)

*THE NASPHV COMPENDIUM COMMITTEE: R. Keith Sikes, DVM, MPH, Chairman; Russell W. Currier, DVM, MPH; Suzanne Jenkins, VMD, MPH; Russell J. Martin, DVM, MPH; Grayson B. Miller, Jr., MD; F. T. Satalowich, DVM, MSPH; James M. Shuler, DVM, MPH. CONSULTANTS TO THE COMMITTEE: Melvin K. Abelseth, DVM, PhD, New York State Department of Health; Kenneth L. Crawford, DVM, MPH; Thomas R. Eng, VMD, MPH, Centers for Disease Control; David A. Espeseth, DVM, Veterinary Biologics Staff, APHIS, U.S. Department of Agriculture; Paul Waters, Representative, Veterinary Biologics Section, Animal Health Institute. ENDORSED BY: Council of State and Territorial Epidemiologists; AVMA Council on Public Health and Regulatory Veterinary Medicine.

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Unless otherwise specified by the product label or package insert, all vaccines must be administered intramuscularly at one site in the thigh. D. Wildlife Vaccination

Vaccination of wildlife is not recommended since no rabies vaccine is licensed for use in wild animals and since there is no evidence that any vaccine will protect wild animals against rabies. It is recommended that neither wild nor exotic animals be kept as pets. Offspring born to wild animals bred with domestic dogs or cats are considered wild animals.

E. Accidental Human Exposure to Vaccine

Accidental inoculation of individuals may occur during administration of animal rabies vaccine. Such exposure to inactivated vaccines constitutes no rabies hazard. No cases of rabies have resulted from needle or other exposure to a licensed modified live-virus vaccine in the United States.

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Anthrax

TABLE II. Notifiable diseases of low frequency, United States

Botulism: Foodborne

Infant

Other

Brucellosis

Cholera

Congenital rubella syndrome

Congenital syphilis, ages < 1 year

Cum. 1988

Leptospirosis (Mass. 1)
Plague

Poliomyelitis, Paralytic
Psittacosis

Rabies, human

Tetanus
Trichinosis

Diphtheria

*There were no cases of internationally imported measles reported for this week.

Cum. 1988

2

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