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HICNet Medical News Digest Mon, 15 Aug 1994 Volume 07 : Issue 36
Today's Topics:
[MMWR 5 Aug 94] Blood Lead Levels
[MMWR] Hantavirus Pulmonary Syndrome
[MMWR] Vaccination Coverage of 2-Year Old Children
Announcements of New Psychology Mailing Lists
Forensic Dentistry Conference
FDA Statement of the Control and Manipulation of Nicotine in Cigarettes
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Lawrence Lee Miller, B.S. Biological Sciences, UCI
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Date: Mon, 15 Aug 94 06:10:16 MST
From: mednews (HICNet Medical News)
To: hicnews
Subject: [MMWR 5 Aug 94] Blood Lead Levels
Message-ID: <T4o4qc1w165w@stat.com>
Blood Lead Levels -- United States, 1988-1991
Since the late 1970s, ongoing contamination of the U.S.
environment by lead has been substantially reduced as major uses of
lead in house paint, gasoline, water-distribution systems, and food
cans have been eliminated or reduced (1). During the 1980s, blood
lead data from both selected populations and convenience samples
indicated a continuation of the decline in blood lead levels (BLLs)
(2) observed during 1976-1980 during the Second National Health and
Nutrition Examination Survey (NHANES II) (3). However, research
during the past two decades has demonstrated adverse health effects
at BLLs previously considered to be safe (1). This report
summarizes estimates of BLLs in the U.S. population from Phase 1 of
the Third National Health and Nutrition Examination Survey (NHANES
III), compares these estimates to those from NHANES II, and
examines demographic patterns of BLLs among children aged 1-5 years
(4,5).
NHANES III is a population-based survey of the health and
nutritional status of the civilian, noninstitutionalized U.S.
population during 1988-1994. Phase 1 data were collected during
October 1988-October 1991. Because blacks and Mexican-Americans*
were oversampled, reliable prevalence estimates could be obtained
for non-Hispanic black and non-Hispanic white persons and for
Mexican-Americans but not for other racial/ethnic groups. Household
interviews and physical examinations were conducted in a mobile
examination center. A 1 mL sample of whole blood was obtained from
each participant aged greater than 1 year. Lead content in whole
blood was measured by graphite furnace atomic absorption
spectrophotometry at CDC. Lead levels below the limit of detection
of 1 ug/dL were assigned a level of 0.5 ug/dL. Software for Survey
Data Analysis (SUDAAN) was used to calculate estimated means,
prevalences, and standard errors that accounted for the sample
weights and complex sample design.
For the U.S. population, the geometric mean (GM) BLL during
1988-1991 was 2.8 ug/dL (95% confidence interval [CI]=2.7-3.0), a
78% decline in the estimated GM BLL since 1976-1980. The decrease
in GM BLL was similar across age groups (Figure 1). As a result,
the cross-sectional age trend in GM BLLs remained virtually
unchanged: the highest GM BLLs were among persons aged 1-2 years
(4.1 ug/dL), and the lowest were among persons aged 12-19 years
(1.6 ug/dL). Among persons aged 20-74 years, GM BLL levels
increased gradually with age.
The prevalence of BLLs greater than or equal to 10 ug/dL among
children aged 1-5 years decreased substantially, from 88.2% during
NHANES II to 8.9% during NHANES III, Phase 1. The prevalence of
elevated BLLs varied by race/ethnicity, income, and residence
(Figure 2). For example, an estimated 35% of non-Hispanic black
children who were poor (i.e., household income less than 1.3 times
the poverty level**) and lived in the central city of a standard
metropolitan statistical area had BLLs greater than or equal to 10
ug/dL, compared with 5% of nonpoor, non-Hispanic white children
living outside of central cities.
The prevalences of BLLs exceeding higher thresholds among
children also decreased. In NHANES II, 53% of children aged 1-5
years had BLLs greater than or equal to 15 ug/dL, and 9.3% had BLLs
greater than or equal to 25 ug/dL. In NHANES III, the prevalences
of children exceeding these same levels decreased to 2.7% (90%
CI=1.7%-3.8%) and 0.5% (90% CI=0.1%-0.9%), respectively.
Reported by: Div of Health Examination Statistics, National Center
for Health Statistics; Div of Environmental Health Laboratory
Sciences and Div of Environmental Hazards and Health Effects,
National Center for Environmental Health, CDC.
Editorial Note: The findings in this report indicate that the
reduction in lead exposure documented during the late 1970s (3)
continued during the 1980s. Reduction in at least two exposure
sources probably contributed most to this decline. First, the
amount of lead used in gasoline declined by 99.8% from 1976 to 1990
(6). Second, the percentage of food and soft-drink cans
manufactured in the United States that contained lead solder
declined from 47% in 1980 to 0.9% in 1990 (7); these two source
reductions have been associated with a reduction of lead in the
typical U.S. diet (8). In addition, reduction in leaded gasoline
probably has resulted in the reduction of the lead content of dust
in and around homes.
Other factors contributing to reduced lead exposure include
the ban on leaded paint for residential use, promulgation of a
standard for lead exposure in industry, the ban on lead-containing
solder in household plumbing, ongoing screening of children and
educational efforts, and lead paint abatement programs in some
jurisdictions. In addition, the number of occupied dwellings built
before 1940, when lead-based paint was commonly used, decreased
from 24.2 million (30.3% of dwellings) in 1980 to 20.8 million
(22.2% of dwellings) in 1989 (9,10). The impact of these changes on
BLLs, although substantial for selected persons and subpopulations,
is unclear for the population as a whole.
Because the developing nervous system is particularly
sensitive to lead toxicity, reducing lead exposure among infants,
toddlers, and preschool children is of particular concern. The
findings in this report indicate that, despite a dramatic decline
in lead exposure among children, approximately 1.7 million children
aged 1-5 years still have BLLs at a level (i.e., greater than or
equal to 10 ug/dL) that can affect cognitive development (1). Poor,
non-Hispanic black children, who reside disproportionately in
center cities, are at increased risk for harmful BLLs. The
demographic pattern of elevated BLLs in children probably reflects,
in part, the distribution of two remaining reservoirs of lead
contamination: 1) deteriorated leaded paint in older housing and 2)
urban soil and dust contaminated by past emissions of leaded
gasoline and by exterior paint on dwellings and other structures
(1).
Further reduction in BLLs among children will require reducing
exposure to lead from these reservoirs, including programs to
safely correct lead hazards in housing and to reduce contact with
lead-contaminated soil and dust. In addition, continued enforcement
of existing standards to reduce lead exposure from other sources
(e.g., drinking water and contaminated dust brought home by
lead-exposed workers) should continue. Because elimination of
remaining lead exposure sources will take many years, ongoing
education of the public is needed about sources of lead exposure
and how to avoid them. Finally, young children should be screened
according to CDC guidelines to identify those children who develop
BLLs high enough to require individualized environmental and
medical intervention.
References
1. CDC. Preventing lead poisoning in young children: a statement by
the Centers for Disease Control. Atlanta: US Department of Health
and Human Services, Public Health Service, 1991.
2. Hayes DB, McElvaine MD, Orbach HG, Fernandez AM, Lyne S, Matte
TD. Long-term trends in blood lead levels among children in
Chicago: relationship to air lead levels. Pediatr 1994;93:195-200.
3. Annest JL, Pirkle JL, Makuc D, Neese JW, Bayse DD, Kovar MG.
Chronological trend in blood lead levels between 1976 and 1980. N
Engl J Med 1983;308:1373-7.
4. Brody DJ, Pirkle JL, Kramer RA, et al. Blood lead levels in the
U.S. population from Phase 1 of the Third National Health and
Nutrition Examination Surveys. JAMA 1994;272:277-83.
5. Pirkle JL, Brody DJ, Gunter EW, et al. The decline in blood lead
levels in the United States: the National Health and Nutrition
Examination Surveys. JAMA 1994;272:284-91.
6. US Environmental Protection Agency. Quarterly summary of lead
phasedown reporting data. Washington, DC: US Environmental
Protection Agency, Office of Mobile Sources, Office of Air and
Radiation, 1991.
7. Can Manufacturers Institute. Food and soft drink can shipments.
Washington, DC: Can Manufacturers Institute, 1992.
8. Bolger PM, Carrington CD, Capar SG, Adams MA. Reductions in
dietary lead exposure in the United States. Chemical Speciation and
Bioavailability 1992;3:31-6.
9. US Department of Commerce/US Department of Housing and Urban
Development. Annual housing survey, 1980: part A. General housing
characteristics. Washington, DC: US Department of Housing and Urban
Development, 1982. (Current housing reports; series H-150-80).
10. US Department of Commerce/US Department of Housing and Urban
Development. American housing survey for the United States in 1989.
Washington, DC: US Department of Housing and Urban Development,
1991. (Current housing reports; series H-150-89).
*Persons residing in survey-sample households who reported their
national origin or ancestry as Mexican/Mexican-American.
**Poverty statistics are based on definitions originated by the
Social Security Administration in 1964, subsequently modified by
the federal interagency committees in 1969 and 1980, and prescribed
by the Office of Management and Budget as the standard to be used
by federal agencies for statistical purposes.
------------------------------
Date: Mon, 15 Aug 94 06:10:59 MST
From: mednews (HICNet Medical News)
To: hicnews
Subject: [MMWR] Hantavirus Pulmonary Syndrome
Message-ID: <15o4qc2w165w@stat.com>
Hantavirus Pulmonary Syndrome -- Northeastern United States, 1994
On January 20, 1994, a 22-year-old Rhode Island man died of
acute respiratory distress approximately 5 hours after
hospitalization. This report summarizes the case investigation.
The man had sought care at an emergency department in Rhode
Island on January 18 complaining of chills and diffuse myalgias and
arthralgias. On evaluation in the emergency department, he had a
temperature of 100.8 F (38.2 C). His complete blood count (CBC)
showed a normal platelet count of 199,000/mm3, a hematocrit of
40.5%, and a white blood cell count of 3600/mm3 with 36% bands. An
acute febrile illness with leukopenia was diagnosed, and he was
discharged to outpatient follow-up. On January 20, he returned to
the emergency department with fever (101.4 F [38.6 C]), increasing
shortness of breath, and cyanosis. He was hypotensive and
hypoxemic, and bilateral pulmonary infiltrates were present on
chest radiograph. His CBC showed thrombocytopenia (61,000/mm3),
elevated hematocrit (50.2%), and a white blood cell count of
17,400/mm3 with 41% bands. His clinical condition deteriorated
rapidly, and he required mechanical ventilation for respiratory
distress. He died later that day.
Because a diagnosis was not established and because the death
occurred less than 24 hours after admission, the case was reported
to the Rhode Island state medical examiner's office. The medical
examiner's office forwarded postmortem blood specimens for
evaluation for hantavirus infection to CDC. Using an enzyme-linked
immunoglobulin M (IgM) capture immunosorbent assay (ELISA),
elevated hantavirus IgM titers were found for the Muerto Canyon
virus (MCV) (proposed to be renamed Sin Nombre virus). Postmortem
tissue samples were positive for hantavirus antigens by
immunohistochemistry. An MCV-like viral sequence was amplified from
lung, spleen, liver, and heart tissues by reverse transcription and
polymerase chain reaction (RT-PCR). A postmortem diagnosis of
hantavirus pulmonary syndrome (HPS) was made. An investigation was
conducted by state, county, and city health departments in New York
and Rhode Island in conjunction with CDC to characterize the
illness and identify the site of exposure and the local rodent
reservoir for the virus.
The patient had not traveled outside the Northeast within the
2 months before his death; he had spent December 1993 and January
1994 in New York and Rhode Island. Epidemiologic and environmental
investigations identified multiple possible exposure sites,
including two warehouses in Queens, New York; a vacation home on
Shelter Island (Long Island); and his family's residence on Long
Island. These sites had a history of rodent infestation within the
past 6 months but had no evidence of current rodent activity. The
patient's apartment in Rhode Island had no history or evidence of
rodent infestation. He had spent 2 weeks in December 1993 cleaning
portions of one of the warehouses in Queens, which had been unused
for more than 10 years. No other persons were involved in this
activity.
Testing was conducted on serum specimens from 64 persons with
exposures similar to that of the patient, including family,
co-workers, and factory workers; no additional cases were
identified. Rodents were captured at all suspected exposure sites
(a total of 19 rodents from all suspected New York sites and 91
from Rhode Island), but none were seropositive for hantavirus.
Trapping will be resumed later in 1994.
Reported by: B Mojica, MD, K Henning, MD, E Bell, New York City
Dept of Health; A Greenberg, MD, R Edstrom, MD, B Smith, Nassau
County Dept of Health, Mineola, Long Island; G Birkhead, MD, S
Kondracki, D White, PhD, New York State Dept of Health. U Bandy,
MD, E Laposata, MD, M Rittmann, W Combs, PhD, B Matyas, MD, State
Epidemiologist, Rhode Island Dept of Health. Div of Vector-Borne
Infectious Diseases and Div of Viral and Rickettsial Diseases,
National Center for Infectious Diseases; Div of Field Epidemiology,
Epidemiology Program Office, CDC.
Editorial Note: As of July 28, 1994, a total of 83 cases of HPS
have been identified in the United States; 45 (54%) of these
patients have died. Ninety-six percent of these cases have been
identified west of the Mississippi River, where Peromyscus
maniculatus (deer mouse) is the primary reservoir of MCV (1-3). The
range of P. maniculatus includes all of the United States, except
the southeast and the Atlantic seaboard. Infected rodents have no
signs of infection; however, they shed virus in their saliva,
urine, and feces. Humans exposed to infected rodent excreta can
develop HPS. The patient in Rhode Island had a history of exposure
to a previously closed space with rodent infestation; such
exposures have been associated with HPS (1). The small number of
rodents caught at suspected exposure sites in New York probably was
attributed to excessively cold weather.
Four cases of HPS have been identified outside the range of P.
maniculatus, one each in eastern Texas, Louisiana, Florida, and
Rhode Island. In Florida, a new but related virus (recently named
Black Creek Canal virus [BCCV]) isolated from Sigmodon hispidus
(cotton rat) is genetically distinct from MCV (4) and from
sequences demonstrated by RT-PCR in lung tissues from a person who
died of HPS in Louisiana (5). Initial serologic testing at CDC of
an acute-phase serum sample from the Florida patient demonstrated
the presence of only immunoglobulin G to MCV by direct ELISA,
although IgM to MCV was detected by the Western blot assay
performed at the University of New Mexico (S. Jenison and B.
Hjelle, University of New Mexico, Albuquerque, personal
communication, 1994) (6). However, repeat serologic testing at CDC
using BCCV antigens showed IgM antibodies. Sequence analysis of the
RT-PCR fragment from lung tissue of the patient in this report
suggests the presence of a variant of MCV or a new, related virus.
Taxonomic assessment of the infecting agent probably will require
identification of the reservoir host and additional sequence
information from viruses in the northeastern United States.
Although the overall incidence of HPS is unknown, the syndrome
appears to be widespread geographically. Recognition of HPS during
its early stages is difficult because of the nonspecificity of
symptoms; later in the syndrome, tachypnea, hemoconcentration,
thrombocytopenia, leukocytosis with a high proportion of bands, and
other features are suggestive of HPS (7,8). Prompt control of
hypoxia (which can rapidly worsen), avoidance of excessive fluid
administration, and the early use of ino-tropic and pressor drugs
appear particularly important in treating HPS (7,8).
CDC has provided intravenous ribavirin for investigational
open-label use in treating HPS since June 1993. On July 19 and 20,
1994, eight experts from outside of CDC reviewed the results of the
open-label ribavirin protocol. Ribavirin was generally well
tolerated in patients with HPS but had no clearly positive
influence on outcome. As a result, enrollment under this protocol
will close September 1, 1994. No controlled studies of this agent
have been conducted in patients with HPS.
Clinicians and public health officials should remain alert for
persons who have unexplained febrile illness with bilateral
interstitial infiltrates, and appropriate specimens should be
collected for serologic and tissue diagnostic assays. Suspected
cases of HPS should be reported to CDC through state health
departments.
References
1. CDC. Hantavirus infection--southwestern United States: interim
recommendations for risk reduction. MMWR 1993;42(no. RR-11).
2. CDC. Hantavirus pulmonary syndrome--United States, 1993. MMWR
1994;43:45-8.
3. Childs JE, Ksiazek TG, Spiropoulou CF, et al. Serologic and
genetic identification of Peromyscus maniculatus as the primary
rodent reservoir for a new hantavirus in the Southwestern United
States. J Infect Dis 1994;169:1271-80.
4. CDC. Newly identified hantavirus--Florida, 1994. MMWR
1994;43:99,105.
5. CDC. Update: hantavirus disease--United States, 1993. MMWR
1993;42:612-4.
6. Jenison S, Yamada T, Morris C, et al. Characterization of human
antibody responses to Four Corners hantavirus infections among
patients with hantavirus pulmonary syndrome. J Virol 1994;68:3000-
6.
7. CDC. Update: hantavirus pulmonary syndrome--United States, 1993.
MMWR 1993;42:816-20.
8. Duchin JS, Koster FT, Peters CJ, et al. Hantavirus pulmonary
syndrome: a clinical description of 17 patients with a newly
recognized disease. New Engl J Med 1994;330:949-55.
------------------------------
Date: Mon, 15 Aug 94 06:11:42 MST
From: mednews (HICNet Medical News)
To: hicnews
Subject: [MMWR] Vaccination Coverage of 2-Year Old Children
Message-ID: <86o4qc3w165w@stat.com>
Vaccination Coverage of 2-Year-Old Children --
United States, Third Quarter, 1993
In 1993, the Childhood Immunization Initiative (CII) was
instituted to increase vaccination coverage among 2-year-old
children to at least 90% by 1996 for four of the five vaccines
routinely recommended for children* and to at least 70% for three
doses of hepatitis B vaccine (1). To monitor progress toward these
goals, national estimates of vaccination coverage are needed. This
report presents national estimates of vaccination coverage among
2-year-old children derived from provisional data from the National
Health Interview Survey (NHIS) for the third quarter of 1993 and
describes the trend in vaccination coverage since 1992, the
baseline year.
The NHIS, a probability sample of the civilian,
noninstitutionalized U.S. population, provides quarterly data to
calculate these national estimates (2). From July through September
1993, the NHIS collected vaccination data from a random sample
(n=483) of survey respondents during household interviews.
Vaccination records were available for the children of 33.7% of
respondents; for 61.1% of respondents, such records were
unavailable and data were based on parental recall. Children's
vaccination history was obtained from both sources by 4.4% of
respondents and was unknown or refused by 0.8%. For data
measurement, 2-year-old children were defined as persons aged 19-35
months at the time of the survey. The children for whom data were
collected were a mean age of 27 months, were born during August
1990-February 1992, and had ranged in age from 2 to 15 months (the
recommended ages for vaccination) sometime during October 1990-May
1993. Data were weighted to provide national estimates. Confidence
intervals were calculated using standard errors generated by the
Software for Survey Data Analysis (SUDAAN) (3).
Compared with 1992 baseline data from the NHIS, data for the
third quarter of 1993 indicate that coverage levels for the
individual vaccinations recommended routinely for children and the
combined series** of vaccinations increased among 2-year-olds
(Table 1) (4). Coverage with three or more doses of vaccine
increased for diphtheria and tetanus toxoids and pertussis vaccine
(DTP)/DT (from 83.0% to 89.9%), for polio vaccine (from 72.4% to
80.4%), for Haemophilus influenzae type b vaccine (Hib) (from 28.2%
to 60.3%), for any measles-containing vaccine (MCV) (from 82.5% to
85.9%), and for the 4:3:1 combined series (from 55.3% to 71.6%).
Baseline data for hepatitis B vaccine were not available. The
increases are statistically significant (p less than 0.05) for all
vaccines (except MCVs) and the 4:3:1 combined series.
Reported by: Assessment Br, Data Management Div, National
Immunization Program; Div of Health Interview Statistics, National
Center for Health Statistics, CDC.
Editorial Note: The findings in this report document an increasing
trend in the level of vaccination coverage in the United States
from 1992 through the third quarter of 1993 and demonstrate
continuing progress toward the 1996 vaccination coverage goal of
the CII. During this period, vaccination levels for DTP, polio
vaccine, and MCVs were the highest ever reported among 2-year-olds
in the United States. However, these levels remain below the CII's
1996 goal of at least 90% coverage. Specifically, an estimated
500,000 U.S. children aged 19-35 months lack at least three doses
of DTP; 1 million need one or more doses of polio vaccine, and
750,000 need one or more doses of an MCV. Overall, only an
estimated 72% of children received the complete 4:3:1 combined
series; therefore, an estimated 1.5 million children need one or
more doses to be fully vaccinated.
The findings in this report are subject to at least one
limitation. Because a substantial proportion of the NHIS data was
based on parental recall, the data may be subject to recall bias or
other reporting errors. Beginning with the 1994 survey, all
vaccination histories will be verified by reviewing provider
records.
Although vaccination levels increased for Hib from 1992
through the third quarter 1993 and for hepatitis B vaccine through
the first three quarters of 1993, coverage with these vaccines
remained substantially low compared with levels for DTP, polio, and
MCV. Two factors may account for the low level of coverage with
three doses of Hib. First, most of the NHIS data in this report
were for children who were born after promulgation of the
recommendations for universal administration of Hib in October 1990
(5). Because nationwide implementation of recommendations does not
occur immediately among providers, the anticipated increase in
vaccination coverage levels often occurs several months to several
years after implementation. Although universal vaccination with Hib
has been fully implemented in the United States, the expected
increase in Hib coverage levels will be adequately reflected only
in future reports. This report documents an increase of 32
percentage points in Hib coverage from 1992 through third quarter
1993. Second, catch-up of children in need of Hib can be
accomplished with fewer than three doses. For example, a
15-month-old child who never received a dose of Hib needs only one
dose. One factor may account for the low level of hepatitis B
coverage. Most of the NHIS data in this report were for children
born before the recommendations for universal hepatitis B
vaccination were promulgated in November 1991 (6). Consequently,
most of these children did not receive this vaccine when they were
the recommended ages for vaccination. To compensate for the time
required to fully implement universal vaccination, the 1996 CII
vaccination coverage goal for hepatitis B vaccine is 70% rather
than 90%.
The reasons for the overall increase in vaccination coverage
levels from 1992 through the third quarter of 1993 are unclear. One
possible explanation is associated with the recent measles epidemic
in the United States during 1989-1991. During and immediately after
the epidemic, a substantial number of the children for whom the
NHIS data in this report were provided were the recommended ages
for routine vaccination. The immediate risk for measles, the
heightened awareness that preschool children needed vaccinations,
and the media's focus on the severity and complications of
vaccine-preventable diseases may have established vaccination as a
high priority among parents and providers (7). As a result, parents
may have intensified efforts to seek vaccinations for their
children and providers may have more consistently sought to
vaccinate children at the earliest recommended ages. However, the
effects of efforts aimed at increasing vaccination coverage during
and/or after an outbreak of vaccine-preventable disease may be
temporary.
The substantial number of undervaccinated children in the
United States and the possibly temporary increases in vaccination
coverage after the recent measles resurgence underscore the
importance of fully implementing the CII, which focuses on 1)
improving delivery, 2) reducing vaccine cost for parents (e.g.,
Vaccines for Children program), 3) raising public and provider
awareness, 4) monitoring coverage and disease, and 5) improving
vaccines and their use. Implementation of this initiative will
assist in further increasing coverage to meet the 1996 goals and
establishing a vaccination-delivery system that can maintain high
coverage levels.
References
1. CDC. Reported vaccine-preventable diseases--United States, 1993,
and the Childhood Immunization Initiative. MMWR 1994;43:57-60.
2. Massey JT, Moore TF, Parsons VL, et al. Design and estimation
for the National Health Interview Survey, 1985-94. Hyattsville,
Maryland: US Department of Health and Human Services, Public Health
Service, CDC, 1989. (Vital and health statistics; series 2, no.
11).
3. Shah BV. Software for Survey Data Analysis (SUDAAN) version 5.5
[Software documentation]. Research Triangle Park, North Carolina:
Research Triangle Institute, 1991.
4. CDC. Vaccination coverage of 2-year-old children--United States,
1992-1993. MMWR 1994; 43:282-3.
5. ACIP. Haemophilus B conjugate vaccines for prevention of
Haemophilus influenzae type B disease among infants and children
two months of age and older: recommendations of the Immunization
Practices Advisory Committee (ACIP). MMWR 1991;40(no. RR-1).
6. ACIP. Hepatitis B virus: a comprehensive strategy for
eliminating transmission in the United States through universal
childhood vaccination--recommendations of the Immunization
Practices Advisory Committee (ACIP). MMWR 1991;40(no. RR-13).
7. CDC. Public-sector vaccination efforts in response to the
resurgence of measles among preschool-aged children--United States,
1989-1991. MMWR 1992;41:522-5.
*At least three doses of diphtheria and tetanus toxoids and
pertussis vaccine (DTP), polio vaccine, and Haemophilus influenzae
type b vaccine (Hib), and one dose of measles-containing vaccine
(MCV) (either measles-mumps-rubella, measles-rubella, or measles
vaccine).
**There are two combined series of vaccinations: the 4:3:1
schedule--four or more doses of DTP/DT, three or more doses of
polio vaccine, and one dose of MCV; and the 3:3:1 schedule-- three
doses of DTP/DT, three or more doses of polio vaccine, and one dose
of MCV.
Monthly Immunization Table
To track progress toward achieving the goals of the Childhood
Immunization Initiative (CII), CDC publishes monthly a tabular
summary of the number of cases of all diseases preventable by
routine childhood vaccination reported during the previous month
and year-to-date (provisional data). In addition, the table
compares provisional data with final data for the previous year and
highlights the number of reported cases among children aged less
than or equal to 5 years, who are the primary focus of CII. Data in
the table are derived from CDC's National Notifiable Diseases
Surveillance System.
------------------------------
Date: Mon, 15 Aug 94 06:12:32 MST
From: mednews (HICNet Medical News)
To: hicnews
Subject: Announcements of New Psychology Mailing Lists
Message-ID: <L8o4qc4w165w@stat.com>
The following announcements of a dozen "InterPsych" lists reated to
psychiatry and psychology were submitted by
Ian Pitchford <I.Pitchford@sheffield.ac.uk>
and general questions may be directed to him.
Lists included:
attachment on mailbase@mailbase.ac.uk
psychiatry-resources on mailbase@mailbase.ac.uk
psychiatry on mailbase@mailbase.ac.uk
depression on mailbase@mailbase.ac.uk
clinical-psychology on mailbase@mailbase.ac.uk
child-psychiatry on mailbase@mailbase.ac.uk
helplessness on mailbase@mailbase.ac.uk
traumatic-stress on mailbase@mailbase.ac.uk
transcultural-psychology on mailbase@mailbase.ac.uk
psychiatry-assessment on mailbase@mailbase.ac.uk
psy-language on mailbase@mailbase.ac.uk
psycho-pharm on listserv@netcom.com
Additional information is provided when you subscribe to one of these
lists. mgh
----------------------------------------------------------------------
attachment on mailbase@mailbase.ac.uk
This list welcomes discussion on Bowlby-Ainsworth's theory of
attachment. From theoretical and philosophical issues, to clinical
or applied issues. Particular emphasis is given to socio-affective
and defensive processes, and unconscious representations.
To join send the message
join attachment firstname lastname
to mailbase@mailbase.ac.uk
Owner: attachment-request@mailbase.ac.uk
----------------------------------------------------------------------
psychiatry-resources on mailbase@mailbase.ac.uk
This list is intended for those who wish to co-operate in the
compilation of a resource guide to enable clinicians and academics in
the areas of psychiatry and abnormal psychology to gain maximum
benefit from the facilities available over the Internet.
To join send the message
join psychiatry-resources firstname lastname
to mailbase@mailbase.ac.uk
Owner: psychiatry-resources-request@mailbase.ac.uk
----------------------------------------------------------------------
psychiatry on mailbase@mailbase.ac.uk
Many research findings and viewpoints in psychiatry are
controversial,leaving a gulf between those pursuing radically
different approaches to mental illness. This forum will act as a
bridge between those taking a biomedical approach and those taking a
psychodynamic approach.
To join send the message
join psychiatry firstname lastname
to mailbase@mailbase.ac.uk
Owner: psychiatry-request@mailbase.ac.uk
----------------------------------------------------------------------
depression on mailbase@mailbase.ac.uk
This forum exists for scholarly discussion of issues related to mood
disorders in clinical and research settings. Integrative biological-
psychological contributions are particularly welcome. Topics include
causation, correlates, consequences, co-morbidity,
treatment/prevention, etc.
To join send the message
join depression firstname lastname
to mailbase@mailbase.ac.uk
Owner: depression-request@mailbase.ac.uk
----------------------------------------------------------------------
clinical-psychology on mailbase@mailbase.ac.uk
This list promotes the exchange of ideas on matters relevant to
clinical psychology, and particularly to the practice of clinical
psychology.
To join send the message
join clinical-psychology firstname lastname
to mailbase@mailbase.ac.uk
Owner: clinical-psychology-request@mailbase.ac.uk
----------------------------------------------------------------------
child-psychiatry on mailbase@mailbase.ac.uk
The Child Psychiatry list is devoted to the discussion of various
issues around Child and Adolescent Psychiatry. This includes
treatment issues, psychopharmacology, inpatient/outpatient care
plans, emergency child/adolescent psychiatry etcetera.
To join send the message
join child-psychiatry firstname lastname
to mailbase@mailbase.ac.uk
Owner: child-psychiatry-request@mailbase.ac.uk
----------------------------------------------------------------------
helplessness on mailbase@mailbase.ac.uk
Learned Helplessness and Explanatory Style was created to discuss the
latest research on animals and humans, biological substratum,
depression, anxiety, prevention, CAVE, politics, children, personal
control, health, battering, bereavement, PTSD, sex differences,
pessimism, work, heritability.
To join send the message
join helplessness firstname lastname
to mailbase@mailbase.ac.uk
Owner: helplessness-request@mailbase.ac.uk
----------------------------------------------------------------------
traumatic-stress on mailbase@mailbase.ac.uk
This list promotes the investigation, assessment, and treatment of
the immediate and long-term psychosocial, biophysiological, and
existential consequences of highly stressful (traumatic) events. Of
special interest are efforts to identify a cure of PTSD
(Post-traumatic Stress Disorder)
To join send the message
join traumatic-stress firstname lastname
to mailbase@mailbase.ac.uk
Owner: traumatic-stress-request@mailbase.ac.uk
----------------------------------------------------------------------
transcultural-psychology on mailbase@mailbase.ac.uk
Discussion of the delivery of mental health services to diverse
cultures. Topics may include, cultural differences in views on
mental disorders, culture-specific syndromes, collaboration between
Western and traditional healers, and cultural variance in symptoms.
To join send the message
join transcultural-psychology firstname lastname
to mailbase@mailbase.ac.uk
Owner: transcultural-psychology-request@mailbase.ac.uk
----------------------------------------------------------------------
psychiatry-assessment on mailbase@mailbase.ac.uk
This sublist focusses on research and clinical issues related to use
of psychological tests (including traditional clinical instruments &
normal personality measures) in psychiatry and clinical psychology.
To join send the message
join psychiatry-assessment firstname lastname
to mailbase@mailbase.ac.uk
Owner: psychiatry-assessment-request@mailbase.ac.uk
----------------------------------------------------------------------
psy-language on mailbase@mailbase.ac.uk
For discussions related to language and psychopathology. Discussions
could include: theories of language and their relevance for the study
of psychopathological speech, new research and publications in the
area, requests for help with one's own research.
To join send the message
join psy-language firstname lastname
to mailbase@mailbase.ac.uk
Owner: psy-language-request@mailbase.ac.uk
----------------------------------------------------------------------
psycho-pharm on listserv@netcom.com Psychopharmacology
The purpose of the Psychopharmacology Mailing List, psycho-pharm,
is to provide a forum for for the professional discussion of all
aspects of clinical psychopharmacology. Clinical psychopharmacology
is broadly defined as the treatment individuals with psychiatric
disorders through the use of psychotropic medications. All mental
health professionals, and graduate students may subscribe to the
Psychopharmacology Mailing List.
To join send the message
subscribe psycho-pharm your-Internet-address
to listserv@netcom.com
PLEASE NOTE: The subscription address AND SYNTAX for the
psycho-pharm list differs from the other InterPsych
lists announced above AND from normal Revised LISTSERV.
Owner: Dr. Ivan Goldberg ikg@phantom.com.
----------------------------------------------------------------------
----------------------------------------------------------------------
Ian Pitchford, c/o Department of Biomedical Science, University of
Sheffield, Western Bank, SHEFFIELD, S10 2TN, United Kingdom.
E-mail: I.Pitchford@Sheffield.ac.uk, md932481@silver.shef.ac.uk
-----------------------------------------------------------------------
For the psychiatry database telnet bubl.bath.ac.uk, login bubl. Search
the subject tree for 616.89 Psychiatry. Contributions welcome.
http://www.bubl.bath.ac.uk/BUBL/home.html (BUBL)
http://mailbase.ac.uk/welcome.html (MAILBASE)
----------------------------------------------------------------------
------------------------------
Date: Mon, 15 Aug 94 06:13:19 MST
From: mednews (HICNet Medical News)
To: hicnews
Subject: Forensic Dentistry Conference
Message-ID: <w9o4qc5w165w@stat.com>
FOR IMMEDIATE RELEASE:
FORENSIC DENTISTRY will be presented 13-17 March 1995 at the Holiday
Inn Crowne Plaza, Rockville, Maryland, USA.
SPONSORS: Armed Forces Institute of Pathology and the American
Registry of Pathology. The formal continuing medical education program
of the AFIP is accepted by the Academy of General Dentistry for
Fellowship, Mastership, and membership maintence credit.
GENERAL INFO: AFIP Education Div.,NW, Washington, DC 20306-6000 USA;
301/427-5231; FAX 301/427-5001; INTERNET: LOWTHER@email.afip.osd.mil
CONTENT: This course is presented by specialist in the fields of
forensic dentistry, criminal investigation, and law. This five-day
course will consist of lectures, a mock trial, illustrative
situations, and student participation in two laboratory exercises
involving the identification of human remains by dental means.
Topics to be covered include:
* AFIP experience with recent forensic missions.
* Mass disaster management.
* Bite mark evidence and analysis.
(including a limited attendance bite mark analysis exercise)**
* New developments in forensic procedures.
* Recording and use of dental data in human identification and
criminal procedures.
** An optional bite mark analysis exercise will be scheduled on
Friday, 17 March 1995 from 3:40 pm until 6:00 pm. There will be NO
additional fee for this session. The session is limited to early
registrants only, prior to 1 February 1995. Enrollment will be
limited to the first 50 paid attendees that request participation.
COURSE DIRECTOR:
Roberet B. Brannon, Col, USAF, DC
TUITION: Early tuition is $595. After 1 February 1995 the tuition is
$625. Active duty military, DoD civilians, full-time permanant
Department of Veterans Affairs employees (not residents or fellows),
and commissioned officers of the Public Health Service with authorized
approval have an early registraion fee of $195. After 1 February 1995,
this fee will be $225.
------------------------------
Date: Mon, 15 Aug 94 06:19:03 MST
From: mednews (HICNet Medical News)
To: hicnews
Subject: FDA Statement of the Control and Manipulation of Nicotine in
Cigarettes
Message-ID: <giP4qc1w165w@stat.com>
STATEMENT BY
DAVID A. KESSLER, M.D.
COMMISSIONER OF FOOD AND DRUGS
on
THE CONTROL AND MANIPULATION
OF NICOTINE IN CIGARETTES
before the
SUBCOMMITTEE ON HEALTH AND THE ENVIRONMENT
COMMITTEE ON ENERGY AND COMMERCE
U.S. HOUSE OF REPRESENTATIVES
JUNE 21, 1994
FOR RELEASE ONLY UPON DELIVERY
In my last appearance before this subcommittee on March 25,
1994, I raised the question of whether the Food and Drug
Administration should regulate nicotine-containing cigarettes as
drugs under the Federal Food, Drug, and Cosmetic Act. A
product is a drug if its manufacturer intends it to be used to
affect the structure or function of the body. Because of the
enormous social consequences of such a decision, we have asked
Congress for guidance as we try to answer this question.
Mr. Chairman, the American public owes a huge debt of
gratitude to this subcommittee for its tireless efforts to focus
attention on this most important public health matter.
Let me begin by summarizing the information that I presented
at that hearing. I reviewed the evidence that supports the
scientific consensus that nicotine is addictive. I also reviewed
the evidence we had at that time on the ability of the tobacco
industry to control nicotine levels, including numerous industry
patents for technologies to manipulate and control nicotine
content. I described activities of the cigarette industry that
resemble those of pharmaceutical manufacturers. I presented
information that raised the question of whether tobaccos were
blended to manipulate and control nicotine levels. And I
provided data showing that over the last decade, nicotine levels
have not dropped in parallel with tar levels -- in fact, they
have risen.
Since March 25th we have continued to focus our analysis and
investigation on the physiological and pharmacological effects of
nicotine and on the degree to which cigarette companies
manipulate and control the level of nicotine in their products.
The information that I presented about industry control and
manipulation of nicotine the last time I testified before you was
suggestive. Today I am going to provide you with actual
instances of control and manipulation of nicotine by some in the
tobacco industry that have been uncovered through painstaking
investigational work over the last three months.
We have discovered that manipulation of nicotine has been
carried out by some even before tobacco seeds were planted in the
fields. We have discovered other forms of manipulation that
occur later, in the design and manufacture of cigarettes.
Today I want to discuss two examples of nicotine
manipulation in some detail. First, we have discovered the
deliberate genetic manipulation of the nicotine content in a
tobacco plant. It is the story of how an American tobacco
company spent more than a decade quietly developing a high-
nicotine tobacco plant, growing it in Central and South America,
and using it in American cigarettes. Second, I will discuss how
chemical compounds are added to cigarettes to manipulate nicotine
delivery.
I. GENETIC MANIPULATION OF NICOTINE CONTENT
The project I am going to tell you about led to development
of a tobacco plant code-named "Y-1." (Chart 1) It has been an
enormous task to piece together the picture of Y-1.
Confidentiality agreements have made getting the facts very
difficult.
The story begins in Portuguese with our discovery of a
Brazilian patent for a new variety of a flue-cured tobacco
plant. (Chart 2) One sentence of its English translation
caught our eye. "The nicotine content of the leaf of this
variety is usually higher than approximately 6% by weight...which
is significantly higher than any normal variety of tobacco grown
commercially." (Chart 3)
Prior to our discovery of the patent, an industry executive
had told us that "flue-cured tobacco naturally contains 2.5 to
3.5 percent nicotine." (Chart 4) Thus, this new specially bred
plant would contain approximately twice the nicotine that
naturally occurs in flue-cured tobacco.
The holder of the Brazilian Y-1 patent was Brown &
Williamson Tobacco Corporation, maker of such cigarettes as Kool,
Viceroy, Richland, Barclay, and Raleigh.
Let me tell you why this discovery interested us. Industry
representatives have repeatedly stated for the public record that
they do not manipulate nicotine levels in cigarettes. The plant
described in this patent represents a dramatic attempt to
manipulate nicotine.
Moreover, when we asked company officials whether plants
were bred specifically for higher nicotine content, we were told
that this was not feasible. We were told that tobacco growers
and cigarette manufacturers have an agreement that the nicotine
level of new varieties of tobacco grown in the United States can
vary only slightly from the levels of standard varieties. Under
this agreement, a new high-nicotine tobacco plant that varied
more than slightly from the standard variety could not be
commercially grown by farmers in the United States.
Nevertheless, we learned that interest in developing a high-
nicotine tobacco plant dates back to at least the mid-1970's. In
1977, Dr. James F. Chaplin, then of both the USDA and North
Carolina State University, stated:
"manufacturers have means of reducing tars but most of
the methods reduce nicotine and other constituents at
the same time. Therefore it may be desirable to
develop levels constant or to develop lines higher in
nicotine so that when the tar and nicotine are reduced
there will still be enough nicotine left to satisfy the
smoker." (Chart 5)
In fact, Dr. Chaplin had been working on genetically
breeding tobacco plants with varying nicotine levels. In a 1977
paper, Dr. Chaplin indicated that tobacco could be bred to
increase nicotine levels, specifically by cross breeding
commercial varieties of tobacco with Nicotiana rustica. N.
rustica is a wild variety, very high in nicotine, but not used
commercially in cigarettes because it is considered too harsh.
Dr. Chaplin has told us that his specially bred plants were
not commercially viable because they did not grow well and
literally did not stand up in the field. Furthermore, he was
surprised that he could not get the nicotine levels as high as he
anticipated. In fact, in his 1977 paper, the highest nicotine
level he reported in these specially bred lines was 3.4 percent
total nicotine, within the normal range for flue-cured tobacco.
At the same time, international efforts focused on
controlling and manipulating nicotine by alternative methods.
For example, the use of reconstituted tobacco:
"... [LTR, a maker of reconstituted tobacco] which
homogenises tobacco for various European cigarette houses
cannot only reduce the tar in the sheet it sends back to
clients; it is able to work into client's scrap and waste
new tobacco of the rustica type, rich in nicotine, in order
to change the relationship of nicotine and tar in the sheet.
It is able to do the same by the alternative method of
adding salts of pure nicotine into the slurry that
eventually becomes tobacco sheet. This is an operation
parallel to, though more exact than, that on which US
geneticists are engaged, in seeking to develop types of
tobacco that are low on tar but fairly rich in nicotine."
Over the next several years Dr. Chaplin continued his
efforts to breed a tobacco plant with a higher nicotine level.
During that time, an employee of a Brown & Williamson-affiliated
company asked Dr. Chaplin for some of his seeds. Some of Dr.
Chaplin's original plant varieties were used as a basis for Brown
& Williamson's work. From what we can gather, there was no
formal release of this high-nicotine tobacco variety for private
use. In the early 1980's, Brown & Williamson grew a number of
different plant lines on its experimental farm in Wilson, North
Carolina, selecting those that had the best agronomic
characteristics.
In 1983, Brown & Williamson contracted with DNA Plant
Technology to work on tobacco breeding. Much of the
developmental work on Y-1 took place in the laboratories,
greenhouses, and fields owned by DNA Plant Technology. After he
retired from USDA, in 1986, Brown & Williamson also hired Dr.
Chaplin as a consultant to work on Y-1 and other projects.
The high-nicotine tobacco variety Y-1 was developed by a
combination of conventional and advanced genetic breeding
techniques. (Chart 6) These include traditional crosses and back
crosses between different plant varieties and more sophisticated
state-of-the-art breeding techniques including anther culture,
(Chart 7) tissue culture, (Chart 8) hybrid sorting, and
protoplast fusion (Chart 9) that resulted in cytoplasmic male
sterility. The genetic makeup of Y-1 was verified by using
genetic engineering techniques involving Restriction Fragment
Length Polymorphism (RFLP). (Chart 10) The value of Y-1 to
Brown & Williamson is reflected in the fact that Brown &
Williamson had DNA Plant Technology make Y-1 into a male sterile
plant. This procedure ensures that when a plant is grown it will
not produce seeds that can be appropriated by others.
Brown & Williamson characterized its achievement in a patent
filing as follows (Chart 11):
"By the present invention or discovery, applicants have
succeeded in developing a tobacco plant that is
agronomically and morphologically suitable for commercial
tobacco production, i.e. it closely resembles SC 58, and
provides a pleasant taste and aroma when included in smoking
tobacco products, yet it is possessed of the N. rustica
high-nicotine attribute. So far as we know, this has not
been accomplished before..." [emphasis in original]
What was accomplished was the development of a tobacco plant with
a high-nicotine content -- about 6 percent -- that grew well and
could be used commercially.
The story of this high-nicotine plant continues in Rio
Grande do Sul, Brazil. (Chart 12) DNA Plant Technology and Dr.
Chaplin both told us they saw Y-1 growing in Brazil in the
1980's. These farms were under contract to Souza Cruz Overseas,
a sister company of Brown & Williamson.
We do not yet have all the details of how Y-1 came to be
growing in Brazil. Until December 13, 1991, export of tobacco
seeds or live tobacco plants was prohibited under Federal law
(Chart 13) unless a Tobacco Seed Plant Export Permit (Form TB-37)
was granted by the United States Department of Agriculture.
Such a permit could be granted only after satisfactory proof was
offered that the seeds or plants were to be used solely for
experimental purposes and then only in amounts of a half a gram
or less.
Brown & Williamson and DNA Plant Technology have each
informed FDA that they believe the other may have been
responsible for the shipment of Y-1 seed outside the U.S. We
have asked both companies to furnish copies of any Tobacco Seed
Plant Export Permits for Y-1.
In reading the Brazilian Y-1 patent, we discovered that two
related applications for the Y-1 variety of a tobacco plant were
filed in the United States. Brown & Williamson filed a U.S.
patent application and a Plant Variety Protection Certificate
Application in 1991. The company also deposited samples of
seeds from this plant with the National Seed Storage Laboratory
in Fort Collins, Colorado.
When we attempted to obtain the Plant Variety Protection
Certificate Application from the U.S. Department of Agriculture,
we learned that the application was withdrawn about 3 months ago,
on March 14, 1994. We were told that Brown & Williamson also
withdrew all seed samples for this variety from the Seed Storage
Laboratory.
We learned that the U.S. patent application had been
rejected by the patent examiner, but that Brown & Williamson
had filed an appeal on February 28, 1994. However, two weeks
later, on March 16, 1994, before receiving a response to their
appeal, Brown & Williamson expressly abandoned the patent.
(Chart 14)
On Friday, June 10, 1994, DNA Plant Technology told us that
it had been authorized by Brown & Williamson to tell FDA that Y-1
was never commercialized.
Mr. Chairman, I wish to submit for the record two invoices
filed with the U.S. Customs Service in 1992. The invoices are
addressed to Brown & Williamson Tobacco Corporation, Louisville,
Kentucky from Souza Cruz Overseas. They refer to "Your Order
Project Y-1" and reveal that more than one-half a million pounds
of Y-1 tobacco were shipped to Brown & Williamson on September
21, 1992.
Four days ago, on Friday June 17, after our questioning of
DNA Plant Technology, and following our letter to Brown &
Williamson indicating that Brown and Williamson had not been
cooperative with our investigation, Brown & Williamson told FDA
that, in fact, three and a half to four million pounds of Y-1
tobacco are currently being stored in company warehouses in the
United States. More significantly, Brown & Williamson revealed
that Y-1 had, in fact, been commercialized.
Mr. Chairman, these brands of cigarettes -- Viceroy King
Size, Viceroy Lights King Size, Richland King Size, Richland
Lights King Size, and Raleigh Lights King Size -- were
manufactured and distributed nationally in 1993 with a tobacco
blend that contains approximately 10 percent of this genetically-
bred high-nicotine tobacco called Y-1. (Chart 15)
When we asked company officials why they were originally
interested in developing a high-nicotine variety of tobacco, they
told FDA that they wanted to be able to reduce tar, while
maintaining nicotine levels.
II. THE CHEMICAL MANIPULATION OF NICOTINE
Let me now move on to the second area. In April, the six
major American cigarette companies released a list of 599
ingredients added to tobacco. Nicotine is not one of the
additives listed. But Mr. Chairman, a number of chemicals on
that list increase the amount of nicotine that is delivered to
the smoker.
Around the time the list was made public, a great deal of
interest was directed toward substances on the list that sounded
particularly toxic. Among those frequently mentioned was
ammonia. Many people may have wondered why the cigarette
industry would add ammonia to tobacco. In fact, there are many
uses of ammonia. Our investigations have revealed an
important one.
Let me refer to a major American tobacco company's 1991
handbook on leaf blending and product development. The handbook
describes two ways that ammonia can be used in cigarette
manufacture. One way is to interact with sugars in the tobacco.
But it is the second way, the effect of ammonia and related
compounds on the delivery of nicotine to the smoker, that is most
striking. Let me quote from that handbook:
"[The ammonia in the cigarette smoke] can liberate free
nicotine from the blend, which is associated with increases
in impact and 'satisfaction' reported by smokers." (Chart
16)
The handbook goes on to describe ammonia as an "impact
booster":
"Ammonia, when added to a tobacco blend, reacts with the
indigenous nicotine salts and liberates free nicotine. As a
result of such change, the ratio of extractable nicotine to
bound nicotine in the smoke may be altered in favor of
extractable nicotine. As we know, extractable nicotine
contributes to impact in cigarette smoke and this is how
ammonia can act as an impact booster." (Chart 17)
This important role that ammonia plays in the liberation of
free nicotine is also emphasized in other parts of the handbook.
"This means that at the same blend alkaloid content, a
cigarette incorporating [ammonia technology] will deliver
more flavor compounds, including nicotine into smoke than
one without it." (Chart 18)
It is important to emphasize here that most of the nicotine
in the average American cigarette is in the bound form. By that
I mean it is not going to readily make its way to the smoker.
Mr. Chairman, I am not going to go into the details of acid-base,
and vapor-phase chemistry, or the bioavailability of nicotine in
the protonated versus the unprotonated form. Suffice it to say
that only a fraction of the nicotine in the tobacco gets inhaled
by the smoker. The handbook indicates that this ammonia
technology enables more nicotine to be delivered to the smoker
than if the ammonia technology is not employed.
What are the ammonia compounds used in this technology? The
company handbook lists a number of different chemical compounds
that can act as "impact boosters." Ammonia compounds known to be
used include diammonium phosphate (DAP), ammonium hydroxide, and
urea. In those countries, such as Germany, that do not allow
DAP, other proprietary formulations are used.
To what are these compounds added? One of the most common
places the ammonia and ammonia-like compounds are applied is to
reconstituted tobacco. When the cigarette is burned, the
reconstituted tobacco serves as a source of ammonia in smoke.
The amount of reconstituted tobacco can be as high as 25 percent
of the tobacco in the cigarette. And we've seen ammonia compound
levels as high as 10 percent in the reconstituted tobacco. Thus,
as the company handbook goes on to state, the benefits of the
reconstituted tobacco:
"come from being an ammonia source, as well as incorporating
sugar-ammonia reactions. As a low alkaloid blend component,
it also absorbs nicotine from higher alkaloid-containing
components. [It thus becomes]...a positive blend
contributor rather than merely a filler."
The handbook also says that ammonia can be applied directly to
the tobacco that goes into cigarettes.
How much additional nicotine does this technology impart?
It is our understanding, based on smoke analysis described in the
company handbook, that an experimental cigarette made of
reconstituted tobacco treated with ammonia has almost double the
nicotine transfer efficiency of tobacco.
How widespread is ammonia use in the industry? The company
handbook states that many U.S. tobacco companies use ammonia
technologies. Until we have access to similar documents from
other companies, we will not know whether other companies use it
directly to affect nicotine levels.
To determine how well nicotine content is controlled in
cigarettes, FDA laboratories compared the content uniformity of
drugs in either tablets or capsules to the content uniformity of
nicotine in cigarettes. What is striking is how little the
nicotine content varies from cigarette to cigarette, suggesting
tight and precise control of the amount of nicotine in
cigarettes. In fact, as this chart shows, the nicotine
content uniformity of the cigarettes tested meets drug content
uniformity standards set by the U.S. Pharmacopeia. (Chart 19)
Mr. Chairman, I have presented information on the control
and manipulation of nicotine because I believe it raises certain
important questions -- questions that are even more important in
light of the repeated assertions of the cigarette industry that
it does not control or manipulate nicotine. Why spend a decade
developing through genetic breeding a high-nicotine tobacco and
adding that tobacco to cigarettes if you are not interested in
controlling and manipulating nicotine? Why focus on the enhanced
delivery of free nicotine to the smoker by chemical manipulation
if you are not interested in controlling and manipulating
nicotine?
III. THE GOALS OF CONTROL AND MANIPULATION
Why is there such interest in controlling and manipulating
nicotine in cigarettes? Senior industry officials are aware that
nicotine is the critical ingredient in cigarettes. Some in the
industry have identified target levels of nicotine necessary to
satisfy smokers' desire for nicotine. And the industry has
undertaken research into nicotine's physiologic and pharmacologic
effects.
Target ranges
Let me give you one example of how a company has identified
specific levels of nicotine necessary to satisfy smokers and
focused on how to achieve those levels. A company document
describes consumer preference testing on "impact," which
according to the company correlates with nicotine. The document
states that impact is a "high priority" attribute of cigarettes
and is:
"...controllable to relatively fine tolerances by product
development/product intervention...(by manipulating nicotine
in blend/smoke...)" (Chart 20)
This document goes on to describe an elaborate model for
establishing the minimum and maximum nicotine levels tolerated by
consumers. It states that the model provides "a median ideal
point level for mg nicotine in smoke" for the population tested
and a range of tolerable nicotine levels around this ideal point.
After applying the testing method to a group of European smokers,
for example, the document concludes:
"It is clear that consumers are less tolerant of
decreases than they are of increases in nicotine
delivery. By the time nicotine level falls to
approximately 0.35mg, 50% of consumers will be saying
that the level of impact is so low they would reject
the product. To reach the equivalent stage of 50% of
consumers rejecting the product as having too high an
impact level, a nicotine level of approximately 5.0mg
would be required. Again, it is important to note that
there is a clear upper as well as lower rejection limit
for nicotine in smoke."
It is thus clear that at least one major cigarette
manufacturer is aware of the need to target nicotine delivery to
levels necessary to satisfy smokers. In fact, as one tobacco
flavor specialist has written, one of the most important goals of
cigarette design is to "ensure high satisfaction from an adequate
level of nicotine per puff," and that even cigarettes with
reduced levels of nicotine and tar must have this property.
Physiologic and pharmacologic effects of nicotine
Publicly available information, including recently released
documents, reveals much about the industry's knowledge of the
drug-like effects of nicotine.
I will begin by describing several studies commissioned by
the tobacco industry. As I go through them Mr. Chairman and
members of the Subcommittee, ask yourselves: Are these the kinds
of studies that would be conducted by an industry interested only
in the flavor or taste of nicotine?
On May 16, 1994, Brown & Williamson made available
previously unreleased results of research that had been conducted
more than thirty years ago. A review of this research, known as
the Project Hippo studies, documents that the industry was
interested in the physiologic and pharmacologic effects of
nicotine as early as 1961.
The first report, known as Project Hippo I, contained an
extensive discussion of the effects of nicotine in the body.
This included, for example, the effects of nicotine on the
central nervous system.
Project Hippo II is an interesting study of what was, in the
early 1960's, the newly evolving field of tranquilizers. Let
me quote from the opening paragraph of the summary of the Final
Report on Project Hippo II:
"The aim of the whole research "HIPPO" was to understand
some of the activities of nicotine - those activities that
could explain why cigarette smokers are so fond of their
habit. It was also our purpose to compare these effects
with those of the new drugs called "tranquilizers", which
might supersede tobacco habits in the near future." (Chart
21)
The comparison of the drug-like effects of nicotine and
tranquilizers was not exactly a well-kept secret. Even in the
1940's you could pick up a magazine and see an advertisement like
this. (Chart 22) What seems to be new about the Hippo study was
that it represented a serious commitment by a tobacco company to
a scientific examination of this pharmacologic property.
Another report released with Hippo and conducted in the
1960's is called "The Fate of Nicotine in the Body." It
reviews the state of knowledge about the distribution of nicotine
in the body and presents the results of studies on nicotine
metabolism in a group of smokers. The report states:
"The numerous effects of nicotine in the body may, at first,
be conveniently measured by various physiological and
pharmacological experiments." (Chart 23)
Other statements reportedly made in this paper speak
directly to the addictive nature of nicotine. The report goes on
to describe what happens when a chronic smoker is denied
nicotine:
"A body left in this unbalanced state craves for renewed
drug intake in order to restore the physiological
equilibrium. This unconscious desire explains the addiction
of the individual to nicotine." (Chart 31)
IV. CONCLUSION
The information that we have presented today has been the
result of painstaking investigation. We now know that a tobacco
company commercially developed a tobacco plant with twice the
nicotine content of standard tobacco, that several million pounds
of this high-nicotine tobacco are currently stored in warehouses,
and that this tobacco was put into cigarettes that have been sold
nationwide. We now know that several tobacco companies add
ammonia compounds to cigarettes, and that one company's documents
confirm that one of the intended purposes of this practice is to
manipulate nicotine delivery to the smoker. And we now know that
some in the industry have identified target ranges of nicotine
delivery. These findings lay to rest any notion that there is no
manipulation and control of nicotine undertaken in the tobacco
industry.
It is equally important to lay to rest, once and for all,
the industry's assertion that nicotine is not addictive. Up
until very recently, the tobacco industry was able to claim that
it did not believe that nicotine was addictive. The release of
company documents, and the testimony of company scientists before
this Subcommittee, has opened a window on what some senior
tobacco officials knew about nicotine's physiological and
addictive properties, as much as 30 years ago.
One important thing that every teenager in this country
needs to know before deciding to smoke his or her first cigarette
is how one cigarette industry official viewed the business of
selling cigarettes:
"We are, then, in the business of selling nicotine, an
addictive drug . . ." (Chart 32)
Thank you.. REFERENCES
1. Kessler, D.A., Statement on Nicotine-Containing Cigarettes.
Testimony before House Subcommittee on Health and the
Environment. March 25, 1994.
2. 21 U.S.C. 321(g)(1).
3. Republican Federativa do Brasil, Institute Nacionel da
Propriedade Industrial, PI 9203690A, "Variendade de fumo
geneticanente estavel e planta de fumo", issued to Brown &
Williamson Tobacco Corporation, June 4, 1993.
4. Brazilian Patent No. PI 9203690A. U.S. Department of State,
Official English translation.
5. Letter of J.W. Johnson, Chief Executive Officer, R.J.
Reynolds Tobacco Company; to D.A. Kessler, Commissioner,
Food and Drug Administration; R.J. Reynolds Tobacco Company,
Winston-Salem, N.C.; February 28, 1994.
6. Chaplin, J.F. Tailoring Tobacco Plants to Meet Future
Demands. World Tobacco October 1978;62:145-9.
7. Chaplin, J.F. Breeding for Varying Levels of Nicotine in
Tobacco. Proceedings from a Symposium on Recent Advances in
the Chemical Composition of Tobacco and Tobacco Smoke,"
Raleigh, N.C., 1977:328-39.
8. [Unidentified Author]. Evolving Techniques of Making
Cigarettes Milder. World Tobacco April 1979:93-101.
9. U.S. patent no. 761,312. "Filing of Utility Patent
Application," Figure 1.
10. U.S. patent no. 761,312, "Appellant's Brief on Appeal,"
at p. 6.
11. 7 U. S. C. 516. (Tobacco Seed and Plant Exportation Act).
12. 7 CFR 34.4(b).
13. DNA Plant Technology did provide a copy of a Phytosanitary
Certificate. This document, which certifies that exported
plants or seeds conform with phytosanitary regulations of
the importing country, was issued to DNA Plant Technology by
U.S. Department of Agriculture, Plant Protection and
Quarantine, to facilitate importation of 20 grams of tobacco
pollen into Brazil. March 20, 1990.
14. U.S. patent no. 761,312, filed September 17, 1991.
15. Plant Variety Protection Certificate Application, PV No.
9100119, filed February 21, 1991, U.S. Department of
Agriculture. (referenced in U.S. patent no. 761,312,
"Filing of Utility Patent Application," at p. 1 - unable to
obtain copy of application from USDA).
16. U.S. patent no. 761,312, "Rejection of Claims," July 10,
1992.
17. U.S. patent no. 761,312, "Appellant's Brief on Appeal,"
filed February 28, 1994.
18. U.S. patent no. 761,312, "Express Abandonment of Patent
Application," filed March 16, 1994.
19. Redacted copies of United States Customs Service Invoices
for Brown & Williamson, dated September 21, 1992.
20. For example, ammonia has been used in efforts to de-
nicotinize cigarettes (U.S. patent no. 4,215,706) and, in
reconstituted tobacco, for its adhesive properties (U.S.
patent no. 5,159,942).
21. Reconstituted tobacco can be made (one of several methods)
by mixing tobacco stems, dust, and other scraps, adding a
liquid solvent to form a "slurry," and then extracting the
liquid and pressing the remaining mixture into a flat sheet.
Almost all U.S. cigarettes contain some reconstituted
tobacco. (Vogues, E. Tobacco Encyclopedia, published by
Tobacco Journal International 1984:389-90.)
22. Food and Drug Administration, Center for Drug Evaluation and
Research, Division of Drug Analysis. Report on analysis of
packages of cigarettes. April 4, 1994.
23. Hertz, A.N. The flavourist's role in the cigarette design
team. World Tobacco March 1985:97-104.
24. Herach, J., Libert, O., Rogg-Effront, C. Final Report on
Project Hippo I. Batelle Memorial Institute, Geneva, for the
British American Tobacco Co. Ltd., January 1962 (released by
Brown & Williamson Tobacco Corp., May 16, 1994).
25. Haselbach, C.H., Libert, O. Final Report on Project Hippo
II. Batelle Memorial Institute, Geneva, for the British
American Tobacco Co. Ltd., March 1963 (released by Brown &
Williamson Tobacco Corp., May 16, 1994).
26. Geissbuhler, H., Haselbach, C. The Fate of Nicotine in the
Body. Batelle Memorial Institute, Geneva, for the British
American Tobacco Co. Ltd., May 1963 (released by Brown &
Williamson Tobacco Corp., May 16, 1994).
27. Gilbert, D.G., Robinson, J.H., Chamberlin C.L., Speilberger,
C.D. Effect of smoking on anxiety, heart rate, and
lateralization of EEG during a stressful movie.
Psychophysiology 1989;26:311-20.
28. Pritchard, W.S. Electroencephalographic effects of
cigarette smoking. Psychopharmacology 1991;104:485-90.
29. Pritchard, W.S., Duke, D.W. Modulation of EEG dimensional
complexity by smoking. J Psychophysiology 1992;6(1):1-10.
30. Pritchard, W.S., Gilbert, D.G., Duke, D.W. Flexible effects
of quantified cigarette-smoke delivery on EEG dimensional
complexity. Psychopharmacology 1993;113:95-102.
31. Meeting. Food and Drug Administration officials; William K.
Dunn, former researcher for Philip Morris, Inc.; and counsel
to Philip Morris, Inc. Law Offices of Hunton & Williams,
Richmond, VA: May 10, 1994.
32. R.J. Reynolds Tobacco Company. New cigarette prototypes
that heat instead of burn tobacco. Chap.7;1988:457-459.
33. U.S. patent no. 3,356,094 C1:8-10.
34. Sir Charles Ellis, Scientific Advisor to the Board of
British-American Tobacco Co., July 1962 (as reported by
Hilts, P.J., in the New York Times, June 16, 1994).
35. Sir Charles Ellis, Scientific Advisor to the Board of
British-American Tobacco Co., July 1962 ( as reported by
Harris, R., for National Public Radio, June 14, 1994).
36. Hutchison, K., Gray, J.A., Massey, H. (chapter authors).
Biographical Memoirs of fellows of the Royal Society of
London: Chapter on Charles Drummond Ellis. by the Royal
Society 1981;Vol.27:199-233.
37. Sir Charles Ellis, Scientific Advisor to the Board of
British-American Tobacco Co., July 1962 (as reported by
Harris, R., for National Public Radio, June 14, 1994).
38. Excerpt from a British-American Tobacco Company research
chronology from June of 1967 (as reported by Hilts, P.J., in
the New York Times, June 17, 1994).
39. Excerpt from a May 30, 1993 British-American Tobacco Company
internal document entitled "Confidential: A tentative
hypothesis on nicotine addiction" (as reported by Hilts,
P.J., in the New York Times, June 17, 1994).
40. Excerpt from a July 1963 Brown & Williamson Tobacco
Corporation internal document, authored by its General
Counsel Addison Yeaman, analyzing whether the company should
acknowledge the hazards of cigarettes or remain quiet (as
reported by Hilts, P.J., in the New York Times, May 7,
1994).
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End of HICNet Medical News Digest V07 Issue #36
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