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PUBLIC HEALTH ASSESSMENT
NEWHALL STREET NEIGHBORHOOD
(a/k/a Bryden and Morse Streets Residential Properties, CERCLIS No. CTN000103143)
(a/k/a Rosem Site Residential Properties, CERCLIS No. CTN000103142)
HAMDEN, NEW HAVEN COUNTY, CONNECTICUT
September 9, 2004


Attachment A: Figure 1

 Figure 1: Extent of Soil Sampling in teh Newhallville Neighborhood, November 2002

Attachment B: Fact Sheets-Ways to Reduce Your Exposure to Soil, Safe Gardening, Summary of Public Health Assessment

What Can I Do To Reduce my Exposure To Soil in my Yard?  [PDF:153KB]
Growing and Eating Fruits and Vegetables in the Newhall Neighborhood of Hamden  [PDF:301KB]
Residential Soils in the Hamden Newhall Street Neighborhood  [PDF:188KB]

Attachment C: Community Health Concerns Interview Form

Confidential Illness Report  [PDF:14KB]

Attachment D: Letter from CT DPH to EPA

Letter from CT DPH to EPA  [PDF:382KB]

Attachment E: CT DPH Cancer Evaluation

CT DPH Cancer Evaluation  [PDF:143KB]

Attachment F: General Toxicological and Epidemiological Information for Lead, Arsenic, and PAHs

Lead

Lead is a naturally-occurring metal in the environment. However, most of the high levels of lead found in the environment come from human activities. Background levels of lead in soil collected from various locations in Hamden (outside the Newhall Street neighborhood) ranged from 35 mg/kg to 360 mg/kg. These levels are consistent with background levels reported in other urban residential areas (ATSDR 1999).

Lead has many uses, most importantly in the production of batteries. Because of health concerns, lead in gasoline, paints, and ceramic products has been dramatically reduced in recent years. However, lead is still present in the environment. People can be exposed to lead from breathing workplace air or dust, eating contaminated foods and drinking contaminated water. Children can be exposed from eating lead-based paint chips or playing in lead-contaminated soil. Lead can affect many organs and systems in the body. The most sensitive is the central nervous system, particularly in children. Lead can cause decreased mental abilities in infants and learning difficulties and reduced growth in young children. Pregnant women exposed to lead can experience premature births and smaller babies (ATSDR 1999). Premature and low birth weight children are more susceptible to various neurological, developmental, learning, behavioral and other chronic health problems such as cerebral palsy, blindness, deafness, slower growth, lower IQ, epilepsy, chronic lung disease, and attention-deficit hyperactivity disorder (Paneth 1995).

In adults, lead exposure (from breathing or swallowing lead) can decrease reaction time, cause weakness in fingers, wrists, or ankles, and possibly affect the memory. Breathing or swallowing lead may cause anemia (a low number of blood cells), may increase blood pressure in middle-aged men, and may affect sperm or damage other parts of the male reproductive system (ATSDR 1999).

With regard to the cancer causing potential of lead, animals that were given very large amounts of lead developed kidney tumors. However, there is not adequate evidence to demonstrate that lead causes cancer in humans (ATSDR 1999).

A blood test is available to measure the amount of lead in a person's blood and to estimate the amount of exposure to lead. Blood tests are routinely used to screen children for potential lead poisoning. The Centers for Disease Control and Prevention (CDC) considers 10 micrograms per deciliter (10 µg/dL) of lead in children's blood to be a level of concern for possible adverse health effects. CT DPH considers 20 µg/dL to be a level of concern for adults.

Arsenic

Arsenic is found in nature at low levels. National background levels of arsenic in soil range from about 1-40 mg/kg, with an average of about 5 mg/kg (ATSDR 2000). Background samples collected in Hamden (outside the Newhall Street neighborhood) ranged from 3-8 mg/kg. People may be exposed to arsenic by eating food, drinking water, breathing air, or through skin contact with soil or water. Children may be exposed to arsenic by playing in soil.

The most characteristic effect of ingesting arsenic for a long period is a pattern of skin changes. These include a darkening of the skin and the appearance of small "corns" or "warts" on the palms, soles, and torso. These skin growths may ultimately develop into skin cancer. Long-term ingestion of arsenic can also lead to damage of the heart and blood vessels and increases the risk of skin, bladder, kidney, liver, and lung cancer. Breathing large amounts of arsenic for a long time increases the risk of lung cancer and can also cause respiratory irritation, nausea and characteristic skin changes. (ATSDR 2000).

The most reliable test for arsenic exposure is a urine test. Since arsenic stays in the body a short time, the test must be done soon after exposure occurs. Tests on hair and fingernails can measure exposure to high levels of arsenic over the past 6-12 months. However, these tests are not very useful for low levels exposures (ATSDR 2000).

PAHs

Polycyclic aromatic hydrocarbons (PAHs) are a group of more than 100 different chemicals that are formed during the incomplete burning of coal, oil, gas, wood, garbage, or other organic substances, such as tobacco and charbroiled meat. PAHs are usually found as a mixture containing two or more compounds and are commonly found in soot or ash.

People are most likely to be exposed to PAHs that are attached to dust or other particles in the air. Sources include cigarette smoke, vehicle exhaust, asphalt roads, and smoke from wood fires. Cooking meat or other food at high temperatures, which happens during grilling or charring, increases the amount of PAHs in the food. National background levels of PAHs found in soil range from less than 1 mg/kg to 60 mg/kg (ATSDR 1995). Background samples in Hamden (outside the Newhall Street neighborhood) for individual PAHs ranged from 0.5 to 4.2 mg/kg. Total PAHs were as high as 12 mg/kg.

PAHs can be harmful to health under some circumstances. Studies on animals have shown that PAHs can cause harmful effects on the skin, and immune and reproductive systems. These effects have not been seen in people. Some PAHs caused cancer in animals when the PAHs were breathed in air (lung cancer), ingested in food (stomach cancer) or applied to the skin (skin cancer). Some people who breathed or touched mixtures of large amounts of PAHs for long periods of time developed cancer (ATSDR 1995).

In the body, PAHs are changed into other chemicals (called metabolites) that can attach to substances within the body. The presence of PAHs attached to these substances can then be measured in body tissues or blood after exposure to PAHs occurs. PAHs or their metabolites can also be measured in urine, blood, or body tissues. Although these tests can show that you have been exposed to PAHs, the tests cannot be used to predict whether any health effects will occur or to determine the extent or source of your exposure to PAHs (ATSDR 1995). Because PAHs are so common in the environment, everyone has some PAHs in their body.

Attachment G: Risk Calculations

Arsenic-Morse Street Group of Properties
  1. Noncancer risks, child aged 1-6 years


    1. Ingestion Dose-Arsenic


    2. This calculation estimates the average daily dose of arsenic to a child, age 1-6 years from incidental soil ingestion.

      ADDingestion = Irc * [Soil] * EF * ED * C1* C2 * 1/BWc * 1/ATnc

      ADDingestion = 100 mg/day * 54 mg/kg * (7 days/week * 39 weeks/year) * 6 years * 10-6 kg/mg * year/365 days * 1/16 kg * 1/6 years = 2.5 E-4 mg/kg/day

    3. Dermal Dose-Arsenic


    4. This calculation estimates the average daily dose of arsenic to a child, age 1-6 years from dermal contact.

      ADDdermal = [Soil] * AF * ABSd * SAc * EF * ED * F * C1* C2 * 1/BWc * 1/ATnc = 54 mg/kg * 0.04 mg/cm2/ev * 0.03 * 3,307 cm2 * (7 days/week * 39 weeks/year) * 6 years * 10-6 kg/mg * year/365 days * 1 ev/day * 1/16 kg * 1/6 year

      ADDdermal = 1E-5 mg/kg/day

    5. Noncancer Hazard Index-Arsenic


    6. HI = ADDingestion +ADDdermal/RfD HI = 2.5 E-4 mg/kg/day + 1 E-5 mg/kg/day = 2.6 E-4 mg/kg/day 2.6 E-4 mg/kg/day/3.4 E-4 mg/kg/day

      HI= 0.76

      A hazard index (HI) of 1 means that the estimated dose is equal to the safe dose. A hazard index less than 1 indicates that the estimated dose is below the safe dose and noncancer health effects are unlikely. A hazard index greater than 1 indicates that the estimated dose exceeds the safe dose and noncancer health effects cannot be ruled out. In this case, the hazard index for arsenic isles than 1. This indicates that noncancer health effects from arsenic are unlikely.

    7. Acute Ingestion dose for a child, aged 2 years


    8. This calculation estimates the average daily dose of arsenic to a child, aged 2 years, from incidental ingestion of soil, assuming a large ingestion rate over a short period (7 days).

      ADDac = IRac * [Soil] * EF * ED * 1/BWac * 1/ATac = 400 mg/day * 54 mg/kg * 10-6 kg/mg * 7 days/week * 1 week * 1/13 kg * 1/7 days = 0.0016 mg/kg/day

      The acute ingestion dose for arsenic exposure for a child is 0.0016 mg/kg/day. ATSDR's acute oral maximum risk level for arsenic is 0.005 mg/kg/day, which is more than the than acute ingestion dose. Therefore, these acute doses are within safe levels and do not pose a significant health threat.


  2. Cancer Risks, Child/Adult Age 1-30 Years


    1. Ingestion Dose-Arsenic


    2. This calculation estimates the lifetime average daily dose of arsenic to a child/adult (age 1-30 years) from ingestion of soil.

      LADDchild ingestion = IRc * [Soil] * EF * ED * C1* C2 * 1/BW * 1/ATc

      LADDchild ingestion = 100 mg/day * 54 mg/kg * (7 days/week * 39 weeks/year) * 6 years * 10-6 kg/mg * year/365 days * 1/16 kg * 1/70 years = 2.16 E-5 mg/kg/day

      LADDadult ingestion = 50 mg/day * 54 mg/kg * 7 days/week * 39 weeks/year * 24 years * 10-6 kg/mg * year/365 days * 1/70 kg * 1/70 years = 9.89 E-6 mg/kg/day

    3. Dermal Dose-Arsenic


    4. This calculation estimates the lifetime average daily dose of arsenic to a child/adult (age 1-30 years) from dermal contact.

      LADDDchild dermal = [Soil] * AF * ABSd * SAc * EF * ED * F * C1 * C2 * 1/BW * 1/ATc = 54 mg/kg * 0.04 mg/cm2/ev * 0.03 * 3,307 cm2 * (7 days/week * 39 weeks/year) * 6 years * 1 event/day * 10-6 kg/mg * year/365 days * 1/16 kg * 1/70 years = 8.5 E-7 mg/kg/day

      LADDDadult dermal = [Soil] * AF * ABSd * SAc * EF * ED * F * C1 * C2 * 1/BW * 1/ATc = 54 mg/kg * 0.01 mg/cm2/ev * 0.03 * 5,672 cm2 * (7 days/week * 39 weeks/year) * 24 years * 1 event/day * 10-6 kg/mg * year/365 days * 1/70 kg * 1/70 years = 3.36 E-7 mg/kg/day

    5. Cancer Risk-Arsenic


    6. ELCR = (LADDchild ingestion + LADDadult ingestion + LADDDchild dermal + LADDDadult dermal) * CSF
      ELCR = (2.16 E-5 + 9.89 E-6 + 8.5 E-7 + 3.36 E-7) * CSF
      ELCR = 3.3 E-5 mg/kg/day * 1.5 (mg/kg/day)-1
      ELCR = 5 E-5


      The estimated lifetime cancer risk (ELCR) for arsenic is 5 E-5 (5 in 100,000). This means that if 100,000 people were exposed to arsenic in soil at the concentration, frequency and duration of exposure assumed in the calculation detailed above, there would be a theoretical increase of five cancers above the number of cancers that would normally be expected to occur in the population of 100,000. Background rates of cancer in the United States are one in two or three (National Cancer Institute, SEER Program 2001). This means that in a population of 100,000, background numbers of cancer cases would be approximately 33,000 to 50,000. Arsenic exposures could result in a theoretical increase of five cancer cases above the background number of 33,000 to 50,000 cancer cases. This represents a relatively low increased cancer risk.
Polycyclic Aromatic Hydrocarbons (PAHs)-Bryden Terrace Group of Properties
  1. Noncancer risks, child aged 1-6 years


    1. Ingestion Dose-PAHS


    2. This calculation estimates the average daily dose of PAHs to a child, age 1-6 years from soil ingestion.

      ADDingestion = 100 mg/day * 30.2 mg/kg * (7 days/week * 39 weeks/year) * 6 years * 10-6 kg/mg * year/365 days * 1/16 kg * 1/6 years = 1.4 E-4 mg/kg/day

    3. Dermal Dose-PAHs


    4. This calculation estimates the average daily dose of PAHs to a child, age 1-6 years from dermal contact with soil.

      ADDdermal = 30.2 mg/kg * 0.04 mg/cm2/ev * 0.13 * 3,307 cm2 * (7 days/week * 39 weeks/year) * 6 years * 1 event/day * 10-6 kg/mg * year/365 days * 1/16 kg * 1/6 years
      ADDdermal = 2.4 E-5 mg/kg/day

    5. Noncancer Hazard Index-PAHs


    6. HI= 1.4 E-4 + 2.4 E-5 /0.02 mg/kg/day
      HI= 1.64 E-4/.02 mg/kg/day
      HI= 0.008

      A hazard index (HI) of 1 means that the estimated dose is equal to the safe dose. A hazard index less than 1 indicates that the estimated dose is less than the safe dose and noncancer health impacts are unlikely. A hazard index greater than 1 indicates that the estimated dose exceeds the safe dose and noncancer health effects cannot be ruled out. In this case, the hazard index for PAHs is well below 1. This indicates that noncancer health effects from PAHs are unlikely.


  2. Cancer Risks, Child/Adult Age 1-30 Years


    1. Ingestion Dose-PAHs


    2. This calculation estimates the lifetime average daily dose of PAHs to a child/adult (age 1-30 years) from soil ingestion.

      LADDchild ingestion = 100 mg/day * 16.04 mg/kg * 7 days/week * 39 weeks/year * 6 years * 10-6 kg/mg * year/365 days* 1/16 kg * 1/70 years = 6.4 E-6 mg/kg/day

      LADDadult ingestion = 50 mg/day * 16.04 mg/kg * 7 days/week *39 weeks/year * 24 years * 10-6 kg/mg * year/365 days * 1/70 kg * 1/70 year = 2.9 E-6 mg/kg/day

    3. Dermal Dose-PAHs


    4. This calculation estimates the lifetime average daily dose of PAHs to a child/adult (age 1-30 years) from dermal contact with soil.

      LADDDchild dermal = 16.04 mg/kg * 0.04 mg/cm2/ev * 0.13 * 3,307 cm2 * (7 days/week * 39 weeks/year) * 6 years * 1 event/day * 10-6 kg/mg * year/365 days * 1/16 kg * 1/70 year = 1.1 E-6 mg/kg/day

      LADDDadult dermal = 16.04 mg/kg * 0.01 mg/cm2/ev * 0.13 * 5,672 cm2 * (7 days/week * 39 weeks/year) * 24 years * 1 event/day * 10-6 kg/mg * year/365 days * 1/70 kg * 1/70 year = 4.3 E-7 mg/kg/day

    5. Cancer Risk-PAHs


    6. ELCR = LADDchild ingestion + LADDadult ingestion + LADDDchild dermal + LADDDadult dermal * CSF
      ELCR = 6.4 E-6 + 2.9 E-6 + 1.1 E-6 + 4.3 E-7 = 1.08 E-5 mg/kg/day * 7.3 (mg/kg/day)-1
      ELCR = 8 E-5

      The estimated lifetime cancer risk (ELCR) for PAHs is 8 E-5 (8 in 100,000). This means that if 100,000 people were exposed to PAHs in soil at the concentration, frequency and duration of exposure assumed in the calculation detailed above, there would be a theoretical increase of eight cancers above the number of cancers that would normally be expected to occur in the population of 100,000. Background rates of cancer in the United States are one in two or three (National Cancer Institute, SEER Program 2001). This means that in a population of 100,000, background numbers of cancer cases would be approximately 33,000 to 50,000. PAH exposures could result in a theoretical increase of 7 cancer cases above the background number of 33,000 to 50,000 cancer cases. This represents a small incremental increased cancer risk.


Definitions for terms used in risk equations:

ABSd = Soil dermal absorption fraction
Arsenic: 0.03, PAHs: 0.13 (EPA 2001)
ADDingestion = average daily dose from ingestion
ADDdermal = average daily dose from dermal contact
ADDac = average daily dose from acute ingestion
AF = skin-soil adherence factor for central tendency residential child; 0.04 mg/cm2/ev (EPA 2001)
skin-soil adherence factor for central tendency residential adult; 0.01 mg/cm2/ev (EPA 2001)
ATnc = averaging time for noncancer risk; 6 years
ATc = averaging time for cancer risk; 70 years
ATac = average time for acute noncancer risk; 7 days
BW = child 50th percentile body weight for age 1-6 years (EPA 1997); 16 kg
BWa = adult 50th percentile body weight (EPA 1997); 70 kg
BWac = body weight, 2-year-old child (EPA 1997); 13 kg
C1 = conversion factor; 10-6 kg/mg
C2 = conversion factor; 1 year/365 days
CSF = cancer slope factor
Arsenic: 1.5 (mg/kg/day)-1 (IRIS)
PAHs: benzo(a)pyrene; 7.3 (mg/kg/day)-1 (IRIS)
ED = exposure duration; 6 years for child, 24 years for adult
EF = exposure frequency; 7 days/week, 39 weeks/year (non-winter weeks)
ELCR = estimated lifetime cancer risk
F = event frequency, 1 event/day
HI = hazard index
IRc = soil ingestion rate for a child; 100 mg/day (EPA 1997)*
IRa = soil ingestion rate for an adult; 50 mg/day (EPA 1997)*
Irac = acute soil ingestion rate for a child (upper percentile) (EPA 1997)
kg = kilograms
LADDchild ingestion = lifetime average daily dose from ingestion for child, aged 1-6 years
LADDadult ingestion = lifetime average daily dose from ingestion for adult, aged 7-18 years
LADDDadult dermal = lifetime average dermal daily dose for child, aged 1-6 years
LADDDchild dermal = lifetime average dermal daily dose for child, aged 7-30 years
mg = milligrams
RfD = EPA reference dose
Arsenic; 3 E-4 mg/kg/day (IRIS)
PAHs: naphthalene used as a surrogate for PAHs; 0.02 mg/kg/day (IRIS)
SAc = Skin surface area, 50th percentile legs, feet, hands, and arms, child aged 1-6 years; 3,307 cm2 (EPA 1997)
SAd = skin surface area, 50th percentile legs, feet, hands, and arms, adult; 5,672 cm2 (EPA 1997)
[Soil] = soil concentration;
Arsenic: 54 mg/kg (95% upper confidence limit of the arithmetic mean)†
PAHs (noncancer calculation): 24.4 mg/kg (total of 95% UCLs for PAHs)
PAHs (cancer calculation): 15.46 mg/kg (total TEF-adjusted 95% UCL for PAHs)


* EPA (1997) recommends using soil ingestion rates of 100 mg/day for child < 6 years and 50 mg/day a child/adult? 6 years. EPA states that these values represent best estimates of average soil ingestion rates. EPA programs have used 200 mg/day and 100 mg/day as conservative estimates of average soil intake rates. CT DPH opted to use the best estimate average values of 100 mg/day and 50 mg/day rather than the more conservative estimates for the sake of consistency with other parameters describing the receptor which are also central estimates (for example, body weight, skin surface area and skin-soil adherence).

† ATSDR (2002) advises using the 95% upper confidence limit of the arithmetic mean. This was performed using Pro UCL (EPA 2001a). A 95% UCL accounts for the variability in the data and ensures that the mean is not underestimated.

Values used to calculate PAH concentrations for cancer and noncancer risk calculations

PAH 95% UCL (mg/kg) Toxic Equivalency Factor (TEF) TEF Adjusted Concentration (mg/kg)
Benzo(a)anthracene 5.2 0.1 0.52
Benzo(b)fluoranthene 5.7 0.1 0.57
Benzo(k)fluoranthene 5.8 0.1 0.58
Benzo(a)pyrene 6.3 1 6.3
Indeno(1,2,3-cd)pyrene 5.7 0.1 0.57
Dibenzo(ah)anthracene 1.5 5 7.5
Total of 95% UCLs 30.2 - 16.04


Attachment H:

ATSDR Conclusion Categories
ATSDR INTERIM PUBLIC HEALTH HAZARD CATEGORIES
Category / definition Data sufficiency Criteria
A. Urgent Public Health Hazard

This category is used for sites where short-term exposures (< 1 year) to hazardous substances or conditions could result in adverse health effects that require rapid intervention.
This determination represents a professional judgment based on critical data which ATSDR has judged sufficient to support a decision. This does not necessarily imply that the available data are complete; in some cases additional data may be required to confirm or further support the decision made. Evaluation of available relevant information* indicates that site-specific conditions or likely exposures have had, are having, or are likely to have in the future, an adverse impact on human health that requires immediate action or intervention. Such site-specific conditions or exposures may include the presence of serious physical or safety hazards.
B. Public Health Hazard

This category is used for sites that pose a public health hazard due to the existence of long-term exposures (> 1 year) to hazardous substance or conditions that could result in adverse health effects.
This determination represents a professional judgment based on critical data which ATSDR has judged sufficient to support a decision. This does not necessarily imply that the available data are complete; in some cases additional data may be required to confirm or further support the decision made. Evaluation of available relevant information* suggests that, under site-specific conditions of exposure, long-term exposures to site-specific contaminants (including radionuclides) have had, are having, or are likely to have in the future, an adverse impact on human health that requires one or more public health interventions. Such site-specific exposures may include the presence of serious physical or safety hazards.
C. Indeterminate Public Health Hazard

This category is used for sites in which "critical" data are insufficient with regard to extent of exposure and/or toxicologic properties at estimated exposure levels.
This determination represents a professional judgment that critical data are missing and ATSDR has judged the data are insufficient to support a decision. This does not necessarily imply all data are incomplete; but that some additional data are required to support a decision. The health assessor must determine, using professional judgment, the "criticality" of such data and the likelihood that the data can be obtained and will be obtained in a timely manner. Where some data are available, even limited data, the health assessor is encouraged to the extent possible to select other hazard categories and to support their decision with clear narrative that explains the limits of the data and the rationale for the decision.
D. No Apparent Public Health Hazard

This category is used for sites where human exposure to contaminated media may be occurring, may have occurred in the past, and/or may occur in the future, but the exposure is not expected to cause any adverse health effects.
This determination represents a professional judgment based on critical data which ATSDR considers sufficient to support a decision. This does not necessarily imply that the available data are complete; in some cases additional data may be required to confirm or further support the decision made. Evaluation of available relevant information* indicates that, under site-specific conditions of exposure, exposures to site-specific contaminants in the past, present, or future are not likely to result in any adverse impact on human health.
E: No Public Health Hazard

This category is used for sites that, because of the absence of exposure, do NOT pose a public health hazard.
Sufficient evidence indicates that no human exposures to contaminated media have occurred, none are now occurring, and none are likely to occur in the future  
* Such as environmental and demographic data; health outcome data; exposure data; community health concerns information; toxicologic, medical, and epidemiologic data; monitoring and management plans


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