MUHLENBERG AND LAURELDALE PENNSYLVANIA

CANCER STUDY: 1996 - 2005

Bureau of Epidemiology
Pennsylvania Department of Health
Harrisburg, Pennsylvania

May 2007
 Muhlenberg Area Cancer Study: 1996 - 2005

Introduction
This report is part of an investigation of cancer in the geographic area defined by the Muhlenberg
School District, in Berks County Pennsylvania. The need for a study grew from reports of cancer among
students who had attended Muhlenberg High School, as well as staff who worked at the school.
Observations of a possible cluster were first noted by area residents starting in the 1990s. Reports of a
cluster lead to the belief that common exposures to ambient agents, both on and off school premises were
occurring, and prompted government officials to look into the situation.

Not knowing if the areas cancer rates were elevated or whether the distribution of cases by time
and space was unusual, the Pennsylvania Department of Health [PADOH] initiated an investigation to
identify cancers among the areas residents, examine the types, and determine the statistical significance
and the epidemiological features of each. To determine the likelihood of a cluster, the incidence rates
were calculated and compared to a set of standard rates represented by the entire state of Pennsylvania. To
objectively measure the cancer burden and determine possible causes of these cases, their distribution was
described, and the medical and epidemiological literature reviewed. The relatively small population being
studied required incorporating cases diagnosed during a ten-year period, from 1996 through 2005.

Methods

Study Population

The principal study population; its geographic boundaries and its size had never been
satisfactorily defined. It is referenced only as former Muhlenberg students and teachers whove been
diagnosed with the disease. In addition to these, area residents who were diagnosed with cancer but did
not fit into either of these groups have also been noted and reported by the community as contributing to
the cluster. Unfortunately, without a clearly defined population at risk, it is not possible to adequately
calculate rates or investigate disease systematically. Typically, the population at risk is defined by the
characteristics of the exposure; the source and distribution in a population. In the current situation this
information is not known. Consequently, the best and only study groups which could be considered for
these analyses were residents of the areas served by the school district, as the likelihood of attendance to
the school is high. For this study, the population at risk is defined as the postal areas which serve

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Muhlenberg Township and Laureldale Borough and correspond to the school district; zip codes 19560
and 19605.

Study Cases

Cases were identified from the files of the Pennsylvania Cancer Registry [PCR] maintained by
the Bureau of Health Statistics and Research at the PADOH. Cases are primary cancers only, and do not
include metastatic cancers that had a point of origin elsewhere in body. Only tumors designated malignant
were included. Cases were studied based on age and year of diagnosis, anatomical site, cell type, and
residence. Anatomical sites and cell types used to classify the cancers were based on definitions
established by the World Health Organization coding scheme described in the, International
Classification of Diseases for Oncology [ICD-O], Third Edition. Because concern centered on young
adults, either of school age or in the years following high school, cases were defined as diagnoses
between ages 15 and 34. Since incidence rates are very low at these ages and the number of annual cases
is small, the period of observation was set as 10 years, from 1996 through 2005, the most current year
statewide data were available.

Analyses

Calculation of Proportionate Distributions

The proportion or percentage a particular cancer type represented among the total number
diagnosed during the study period was calculated. Percentages are shown for 23 types and ALL OTHERS.
The frequency distribution is based on a total of 37 incident cases diagnosed for the years 1996 through
2005. Because of data restrictions, for Pennsylvania the years 1996 through 2004 were used to describe
the proportionate distribution of types during the same period. These are shown in Table 1. There were
14,644 total invasive cases.

Calculation of Risk

Rates were evaluated by calculating a statistic called the standardized incidence ratio [SIR], often
referred to as the Risk Ratio. The SIR provides a measure of the cancer incidence rate relative to the state.
The number of new cases that occurred (observed) in the study area was compared to the number that
would be expected (expected), where the ratio or SIR = Cancers Observed / Cancers Expected. Expected
cases were determined by multiplying the study population by the statewide incidence rate. These were
calculated for individual age groups 15-19, 20-24, and 25-34, and totaled.

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 Statistical Evaluations

Table 2 shows the standardized incidence ratios for major types and the categories ALL OTHERS,
and ALL CANCERS, across the ten-year period, 1996 to 2005. A Risk Ratio or SIR of one (1.00) or near
one indicates that the number of new cancers observed is the same as the number expected, and suggests
the cancer risks are the same. A ratio greater than 1.00 indicates the number of new cases observed is
more than the number expected, and suggests the cancer risk is greater than the state. A ratio less than
1.00 indicates the number of new cases is fewer than expected, and the cancer risk is lower than the state.
The ratios are only estimates of the risk in the study area relative to Pennsylvania.

Though the incidence ratio suggests a certain risk, it must be evaluated to determine if the ratio is
statistically significant. A ratio is considered significant (higher or lower than 1.00) if the 95 percent
confidence interval for the ratio does not include 1.00, based on the Poisson distribution.

Results

Proportionate Distribution

Table 1 shows the numbers of new cases (incidence) for each cancer and their proportion of the
total number expressed as percentages. Over the 10 year period (1996-2005) 37 new cancers were
diagnosed among the areas residents ages 15 to 34. The most common types were testicular cancer (6)
malignant melanoma of the skin (5), thyroid cancer (5), and Hodgkins lymphoma (4). This is also shown
by the pie chart in Figure 1. During the 1996 to 2004 period 14,644 new cases were diagnosed in
Pennsylvania. The distribution of the types compared to that for the entire state is very similar. The
leading cancers were thyroid cancer, malignant melanoma of the skin, testicular cancer, and non-
Hodgkins lymphomas. However, both these distributions differed from older residents where colon-
rectum, lung, breast and prostate cancers account for 60 percent of the total number.

Rates

Rates are expressed as the ratio of the number of cancers that occurred to the number expected,
using the method called indirect age-adjustment. Table 2 shows the number of cancers that were
diagnosed and the number of cases that would be expected to occur if the study areas cancer rate was
identical to Pennsylvanias rate. While a total of 37 cancers were diagnosed only 27 were expected. The

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risk ratio or SIR for the two zip codes combined was 1.37 [37 obs. / 27.04 exp. = 1.37] and suggests the
rate for the zip codes was 37 percent higher than statewide. Yet, the size of the ratios based on the small
numbers of observed cases (37), cannot be considered statistically significant. Individual cancer types
with a ratio greater than 1.00 were colon-rectum, malignant melanoma, cervix, testicular cancer, kidney,
thyroid cancer, non-Hodgkins lymphoma, and Hodgkins lymphoma (Table 2). However, these are based
on very small numbers and the likelihood that variations in the incidence of 3 or fewer cases could be do
to chance is large; therefore they are not considered statistically significant.

Discussion

To identify a relationship between cancer incidence in these communities and environmental

factors the epidemiological features of the most diagnosed types were reviewed. These are described here.

Risk Factors

Thyroid cancer has many known risk factors. External acute childhood x-radiation is
carcinogenic for long periods of time. Both iodine deficiency and iodine excess can increase thyroid
cancer risk. Cruciferous vegetables appear to be protective, while seafood may increase risk. There
appears to be some association with breast cancer. The influence of estrogens and other hormones may
affect risk. Other than those noted there are no other environmental causes of thyroid cancer.

Malignant melanoma-of-the-skin varies by the amount of sun exposure, particularly early in life.
Severe burns are a known risk factor. Persons less pigmented who burn easily are at greatest risk.
Atypical moles or dysplastic nevi appear to be an important precursor lesion in cancer development. In
some individuals the risk of nevi is transmitted as an autosomal dominant trait, which can lead to clusters
in families. Hormonal factors play a role in tumor growth, but their role in tumor development is not
clear.

Testicular cancer risk is nearly zero before puberty and after age 60. Because this cancer is
diagnosed at such a young age, it probably develops over time, starting very early in life. Clearly, rising
hormones during puberty contribute to the growth of the cancer. Investigations of tobacco use, diet and
alcohol have not revealed any relationship to risk. Investigations of its cause(s) have addressed a large
number of possible risk factors; reproductive factors and hormones, fertility, body frame, tobacco use,
diet and alcohol, infections, immunosuppresion, ionizing radiation, medical conditions, and prenatal
exposures. No relationship has been found for tobacco, alcohol or diet. One of the main hypotheses being
explored is that the cancer may have a viral etiology. Mumps can cause orchitis or inflammation of the
gonads and there is consistent evidence that mumps infection increases the risk of this cancer. Other

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infectious agents considered are Epstein-Barr virus and cytomegalovirus; both have also been shown to be
associated. However, no environmental agent has not yet been identified.

Non-Hodgkins lymphoma represents a large number of cancers involving lymph tissues. While
radiation can cause leukemia, few studies suggest an increased risk of lymphomas from radiation. Since
viruses are known to cause lymphoma in a variety of animal models, it has been suspected that they play a
role in the development of non-Hodgkin's lymphoma. Clearly HTLV-1 can cause lymphomas, in addition
to leukemia, but these are relatively rare infections, and the virus contributes very little to the overall
population-based rates. In addition, the Epstein-Barr virus (which causes mononucleosis) contributes to
Hodgkin's lymphoma but, not to non-Hodgkin's lymphomas. Vaccination with BCG for Tuberculosis
prevention has also been shown to cause lymphomas, as a result of chronic lymphatic stimulation. Since
numerous animal leukemia viruses can cause chronic lymphatic stimulation in animals leading to
lymphoma, a similar model involving animal viruses infecting humans might occur.

Cervical cancer is a neoplastic growth that arises as the result of infection from the Human
papillomavirus, known to cause warts. Types 16 and 18 are believed to be two principal agents. Typically
this is a disease of adults, but it can develop in adolescents. The virus is spread by person-to-person
transmission. It is very slow growing and can take ten years or more for cancer to develop and become
clinically evident. While the infection is not that uncommon, few progress to invasive disease if women
receive periodic screening or PAP tests. A low rate of PAP testing in certain groups of women at younger
ages can result in the appearance of higher rates years later.

Breast cancer is the leading cancer in Pennsylvania. About 10,000 new cases are diagnosed
annually. Risk is largely determined by years of exposure to estrogen. The earlier menarche starts and the
later in life menopause begins the more ovulatory cycles and exposures to estrogen, while suppression of
ovulation during pregnancy and from breast-feeding lowers the risk. Consequently, the earlier in life
childbearing begins the lower the risk. Breast cancer occurring under age 40 indicates a strong genetic
component independent of other risk factors. Relative to the environment, medical and epidemiological
research has not demonstrated an environmental cause to breast cancer. This includes air pollution,
electromagnetic radiation, radon, and ambient pollutants inside and outside the house, including drinking
water. The only identified environmental risk factor is ionizing radiation. However, exposures would have
to be extremely large to elevate the cancer rates in a population, such as a nuclear accident.

Leukemia represents about two percent of all new cancers. The relationship of leukemia and the
environment is not clear. Little is known about the factors responsible for the development of most types
of leukemia. And only in rare circumstances can one say with certainty that an occurrence is due to a

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specific agent. Ionizing radiation is a good example. Large cohort studies of Atomic Bomb survivors and
studies of excess exposures in the United States have shown extraordinarily high rates, and have made
possible the determination of a dose-response curve. Benzene is another established human
leukemogenic agent. This is based on experimental studies and on numerous investigations of job related
exposures to workers during chemical manufacturing, petroleum refinery, and from the manufacturing of
shoes, leather, and rubber products. The role of viruses in the cause of leukemia in animals has been
established for a long time. More recently, the human T-cell lymphotropic virus (HTLV-1) has been
shown to cause some adult T-cell leukemia. In addition, therapeutic agents such as chemotherapy
(alkylating agents) and diagnostic x-rays (if not controlled) can cause leukemia.

In the absence of a valid hypothesis or description of a specific environmental insult resulting in

human exposures, it was not possible to evaluate a factor that might potentially be attributable to the
incidence of cancer in these communities. What is known is that for cancer to be attributed to an
environmental agent the following conditions must be met: 1) the agent must be a proven human
carcinogen; 2) there must be a pathway of exposure to the population that results in an exposure, 3) it
must be at a dose sufficiently large to induce disease, and 4) the duration of the exposure must be long
enough to result in cancer. Neither a specific agent nor any of these conditions have been described.
What is known about the etiology of the particular cancers addressed in this investigation does not
support the idea that the school facilities or the area surrounding them is responsible for their occurrence.

Conclusion
The Pennsylvania Department of Health is sensitive to the communities concerns about the rates
of cancer in young adults in the Muhlenberg - Laureldale area, and the safety of their environment. To
provide the most current assessment of the cancer burden and risks, the PADOH examined the types of
cancer, their relative frequencies, as well as the incidence rates, for the ten-year period, 1996-2005. This
was not an etiological investigation, designed to prove that an environmental pollutant can cause cancer;
rather, it was a descriptive study. It provided objective measures of cancer risks relative to all
Pennsylvanians. When compared to the state, the distribution of types was essentially the same, and
cancer risks as measured by the incidence rates, were not found to be significantly different from the
states rates. Based on the types of cancer in the area and the rates, there isnt an indication that the
environment contributed to the cancer rates, and there are no environmental data demonstrating there
were human exposures to carcinogens in the area that could increase the risk.