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PETITIONED HEALTH CONSULTATION

Public Comment Release

Review of Groundwater Sampling Results from the Myrtle Grove Trailer Park Well System

MYRTLE GROVE TRAILER PARK
PLAQUEMINE, IBERVILLE PARISH, LOUISIANA


APPENDIX A: FIGURES

Myrtle Grove Trailer Park Site Location Map
Figure 1. Myrtle Grove Trailer Park Site Location Map

Demographic Statistics Within One Mile of the Myrtle Grove Trailer Park Site
Figure 2. Demographic Statistics Within One Mile of the Myrtle Grove Trailer Park Site


APPENDIX B: TABLES

Table 1.

Exposure Pathway Elements Myrtle Grove Trailer Park Plaquemine, Louisiana
Pathway Name Exposure Pathway Elements Time Frame
Source Media Point of Exposure Route of Exposure Exposed Population
Completed Exposure Pathways
Groundwater Unknown MGTP Well System On site Ingestion; Dermal; Inhalation Residents of the MGTP Past
Eliminated Exposure Pathways
Groundwater Unknown MGTP Well System On site None None Current

MGTP = Myrtle Grove Trailer Park


Table 2.

Vinyl Chloride Concentrations in the Myrtle Grove Trailer Park Well System Plaquemine, Louisiana
Sample Collection Date Well Head 1 -
Vinyl Chloride Concentrations (ppb)
Well Head 2 -
Vinyl Chloride Concentrations (ppb)
Distribution System -
Vinyl Chloride Concentrations (ppb)
April 11, 1994ND (0.10)ND (0.10)NA
November 5, 19974.96.3NA
September 30, 199813.9*11.0*NA
February 26, 200111.28.45NA
March 13, 200110.410.3NA
March 20, 2001NANA13.8

Source: LDHH, 2002.

* QC out of control.

NA = Not available because no sample was collected
ND = Not detected (value in parenthesis is the minimum detection limit)
ppb = Parts per billion


Table 3.

Myrtle Grove Trailer Park Well System Sampling Data Plaquemine, Louisiana
Compound Well Head 1 -
Concentration Range (ppb)
Well Head 2 -
Concentration Range (ppb)
Distribution System -
Concentration Range (ppb)
BromodichloromethaneND (0.10)ND (0.10)3.1 - 20.6
BromoformND (0.23)ND (0.23)16.0* - 16.9
ChlorodibromomethaneND (0.24)ND (0.24)28.6 - 30.2
ChloroformND (0.09)0.810.3 - 13.0
cis-1,2-Dichloroethylene1.4 - 2.021.0 - 2.072.16

Source: LDHH, 2002.

* QC out of control for this analyte

ND = Not detected (value in parenthesis is the component minimum detection limit from the 2001 sampling events)
ppb = Parts per billion


APPENDIX C: VINYL CHLORIDE ORAL EXPOSURE

The text in this appendix provides additional information concerning ATSDR's toxicologicevaluation of vinyl chloride exposures via the oral route.

The maximum concentration of vinyl chloride recorded in drinking water at MGTP (13.8 ppb) would correspond to maximum doses of 1.38 micrograms per kilogram per day (µg/kg/day) for a 10-kilogram (kg) child drinking 1 liter per day (L/day) and 0.39 µg/kg/day for a 70-kg adult assuming consumption of 2 L/day.

Based on animal studies by Til et al. (1983, 1991), EPA derived a chronic oral reference dose (RfD) of 3 µg/kg/day. This RfD was based on a human equivalent NOAEL (no-observed-adverse-effect level) of 90 µg/kg/day for noncancerous liver cell polymorphism and a safety factor of 30. EPA derived this human NOAEL from a rat NOAEL of 130 µg/kg/day for the same effect, using a PBPK (physiologically based pharmokinetic) model that allowed improved calculation of the human dose that would be expected to result in the same level of toxicity as that observed in animals (IRIS 2002).

The dose received by an adult drinking this water would be 0.39 µg/kg/day, which is only 0.4% of the human equivalent NOAEL calculated by the EPA. The corresponding dose for a child (1.38 µg/kg/day) would be 1.5% of that human NOAEL.

Vinyl chloride is a known human carcinogen under certain circumstances. Vinyl chloride hasbeen consistently associated with elevated incidences of rare angiosarcomas of the liver inhumans, but only by inhalation and only at the extremely high occupational exposures that wereonce associated with certain job categories, mainly autoclave cleaners hired before 1970(Zocchetti 2001). However, due to improvements in industrial hygiene made decades ago, theseextremely high exposures no longer occur, even in occupational settings. Nevertheless,angiosarcoma of the liver still occurs at an extremely low rate in the general population (0.5-2.5cases per 10,000,000) (Zocchetti 2001). But its cause remains largely unknown.

There are no drinking water studies of vinyl chloride exposure in humans (ATSDR 1997).However, the scientific literature contains no evidence of a strong relationship betweennonoccupational, environmental exposure to vinyl chloride and angiosarcoma of the liver or anyother cancer (Zocchetti 2001, Ward et al. 2001). In particular, there is no evidence that vinylchloride in drinking water, at doses that are achievable outside the laboratory, can cause cancer inhumans via the oral route.

However, at sufficiently high oral doses, vinyl chloride does cause hepatic angiosarcoma in animals. The lowest recorded cancer effect level (CEL) in laboratory animals exposed orally to vinyl chloride in oil is 300 µg/kg/day for liver angiosarcoma in Sprague-Dawley rats treated by gavage(1) 5 times a week for a year, i.e., one-third to one-half the animals' lifetime (ATSDR 1997). In humans, this dose would be numerically (if not biologically) equivalent to 10,500 ppb in drinking water for an average 70-kg adult drinking 2 L/day, or 3,000 ppb for a 10-kg child drinking 1 L/day, for several decades. These levels are over 650 times higher than the maximum recorded level of vinyl chloride in the MGTP well system, and the residents were not exposed for decades. If one assumes that sufficiently high oral doses of vinyl chloride could induce cancer in humans, such high doses are evidently unattainable outside the laboratory. Based on all of the information in the preceding text, it is unlikely that even the highest level of vinyl chloride detected in drinking water at MGTP would have been high enough to produce any clinically significant adverse health effects in humans, even after a lifetime of chronic oral exposure. Nevertheless, because EPA's federal safe drinking water standards are legally enforceable, the residents of MGTP were provided with an alternative source of drinking water, as a prudent (i.e., conservative) public health measure.

References:

ATSDR 1997. Toxicological Profile for Vinyl Chloride (Update). Atlanta, Georgia: U.S.Department of Health and Human Services, Public Health Service, Agency for Toxic Substancesand Disease Registry. September 1997.

IRIS 2002. Integrated Risk Information System, http://www.epa.gov/iris/index.html, an on-linedatabase developed and maintained by the United States Environmental Protection Agency, File -Vinyl Chloride (CASRN 75-01-4) http://www.epa.gov/iris/subst/1001.htm.

Til HP, Immel HR, Feron,VJ. 1983. Lifespan oral carcinogenicity study of vinyl chloride in rats.Final report. CIVO Institutes. TNO Report No. V 83.285/291099, TSCATS DocumentFYI-AX-0184-0353, Fiche No. 0353.

Til HP, Feron VJ, and Immel HR. 1991. Lifetime (149 week) oral carcinogenicity study of vinylchloride in rats. Food Chemistry and Toxicology 29: 713-718.

Ward E, Boffetta P, Andersen A, Colin D, Comba P, Deddens JA, De Santis M, Engholm G,Hagmar L, Langard S, Lundberg I, McElvenny D, Pirastu R, Sali D, Simonato L. 2001. Updateof the follow-up of mortality and cancer incidence among European workers employed in thevinyl chloride industry. Epidemiology 2001 Nov;12(6):710-8.

Zocchetti C. 2001. Liver angiosarcoma in humans: Epidemiological considerations, Med Lav2001 Jan-Feb 92(1):39-53 (Italian). An English abstract of this review article is available onlineat http://www.ncbi.nlm.nih.gov/entrez/.


APPENDIX D: DOSE CALCULATIONS

Vinyl Chloride Exposure from Showering

When showering in contaminated water, a resident may be exposed from (1) breathing theportion of the contaminant that is released into the air and (2) absorbing the contaminant throughthe skin. In addition, a resident could inhale the contaminant in the vapor while showering andwhile standing in the bathroom immediately after showering. Inhalation and dermal exposures tovolatile organic compounds (VOCs) in the shower or bath may each be equal to or exceedexposures from ingestion of the contaminated drinking water (Jo et al. 1990; Andelman et al.1990b; Mattie et al. 1994; Kezic et al. 1997; Kerger & Paustenbach 2000).

ATSDR made the following conservative assumptions to estimate "worst case" vinyl chlorideexposure for residents who shower with water contaminated with vinyl chloride.

  1. A resident would take a 10-minute shower once every day
  2. A resident would spend an additional 15 minutes in the bathroom after showering
  3. The concentration of vinyl chloride in the bathroom both during and after showering (i.e., throughout the entire 25 minutes of exposure) would be constant and equal to the maximum concentration achieved during showering
  4. The rates of volatilization for vinyl chloride are similar to the rates for chloroform and trichloroethylene, and
  5. The rate of skin absorption of vinyl chloride is similar to the rate for chloroform absorption.

The maximum concentration of vinyl chloride in the bathroom air can be estimated by use ofsimple one-compartment modeling. This concentration can be estimated using the followingmathematical equation (Andelman 1990a):

C sub a equals C sub w times f times F sub w times t divided by V sub a

where:
Ca bathroom air concentration in milligrams per cubic meter (mg/m3)
Cw tap water concentration in milligrams per liter (mg/L)
f fractional volatilization rate (unitless)
Fw shower water flow rate in liters per minute (L/min)
t exposure time in minutes (min)
Va bathroom volume in cubic meters (m3)

The above equation for calculating the air concentration in the bathroom will be evaluated using a conservative approach by assuming a fractional volatilization rate (f) of 0.9, a flow rate (Fw) in the shower of 8 L/min, and an approximate volume (Va) of a small bathroom of 10 m3. Also, the maximum concentration of vinyl chloride detected in the well system' distribution line (approximately 0.014 mg/L) will be used as the concentration in tap water (Cw). Using these values, the maximum concentration of vinyl chloride attained in the bathroom during showering would be calculated as follows:

Ca = 0.014 mg/L 0.9 8 L/min 10 min = 0.1008 mg/m3
10 m3

For purposes of conservatism (and ease of calculation), we will assume that this maximumconcentration of 0.1 mg/m3 or 0.04 parts per million (ppm) (1 ppm vinyl chloride = 2.6 mg/m3) issustained throughout the next 15 minutes during which time the bather is still being exposed. (Inreality, the maximum concentration would be reached only toward the end of showering and wouldrapidly decline shortly after the shower was turned off.) Based on the equation above and theindicated assumptions, if the concentration of vinyl chloride in the shower water is 0.014 mg/L, thenthe maximum concentration of vinyl chloride attained in the bathroom air during showering wouldbe 0.1 mg/m3 or 0.04 ppm.

Inhalation exposures in the shower and bathroom can be estimated using the following equation:

E sub i equals C sub a times B times t sub i

where:
Ei inhalation exposure in milligrams (mg)
Ca bathroom air concentration in milligrams per cubic meter (mg/m3)
B breathing rate in cubic meters per hour (m3/hr)
ti exposure time in hours (hr)

Assuming an adult breathes 1.0 cubic meter (m3) of air per hour and the bathroom air concentration (as estimated previously) is 0.1 mg/m3, the estimated exposure from showering and use of the bathroom after showering are as follows:

shower inhalation dose = (0.1 mg/m3) (1.0 m3/hr) (10/60 hr) = 0.02 mg

bathroom inhalation dose = (0.1 mg/m3) (1.0 m3/hr) (15/60 hr) = 0.025 mg

Studies in humans have demonstrated that the dermal absorption dose of a chlorinated volatileorganic compound is comparable to the shower inhalation dose (Wan et al. 1990). Thus, in the present case, we may further assume that

shower dermal dose = shower inhalation dose = 0.02 mg

The total exposure to vinyl chloride is, therefore, the sum of the three exposures calculated above:

total dose = showerinh + bathroominh + showerder = 0.065 mg

This model estimates worst-case air concentrations because (1) it does not account for dilutionfrom ventilation in the bathroom, and (2) it assumes exposure occurs at a maximum airconcentration throughout duration of the bathroom use. In fact, the vinyl chloride concentrationwill gradually increase to a maximum at the end of the shower and it will gradually decrease oncethe shower is turned off. Thus, the maximum concentration will actually be sustained for but afraction of the total exposure event.

In conclusion, based on the assumptions specified above, if the measured tap water concentrationwere 0.014 mg/L, then the estimated maximum bathroom exposure to vinyl chloride during andafter showering would be 0.0009 mg/kg/day for a 70-kg adult. By comparison, the ingestion (i.e.,drinking water) exposure dose (assuming an ingestion rate of 2 L/day) would be 0.0004mg/kg/day. The lowest known oral effect levels for vinyl chloride are 2-3 orders of magnitudehigher than the maximum estimated total exposure (0.0013 mg/kg/day) in this scenario (ATSDR1997). All known inhalation effect levels are higher, still.

Vinyl Chloride Exposure From Other Activities

Although a bath would result in much less volatilization of VOCs than would showering,ATSDR assumed that bathing and showering would both result in the same maximumconcentration of vinyl chloride in air of 40 ppb (0.04 ppm). Due to the conservative nature of theassumptions made, the model tends to overpredict the actual levels of vinyl chloride vaporsduring showering (Williams et al. 2000). Household exposures (cooking, washing dishes, and soon) are much less than showering because the flow rate of water from a kitchen faucet is muchless than in the shower, the volatilization rate is much less, and the size of the kitchen area ismost likely much larger than the bathroom area. All of these factors will decrease the exposure.Outdoor exposures (such as swimming in pools or playing in sprinklers) are also much less thanshowering for these same reasons. Therefore, 0.04 ppm (40 ppb) is used as the maximum site-specific concentration of vinyl chloride in air.

References

Andelman JB. 1985. Inhalation exposure in the home to volatile organic contaminants ofdrinking water. The Science of the Total Environment. 47: 443-460.

Andelman JB. 1990a. Total Exposure to Volatile Organic Compounds in Potable Water. In: Significance and Treatment of Volatile Organic Compounds in Water Supplies; Chapter 20. Lewis Publishers. Chelsea, MI. 485-504.

Andelman JB, Giardino NJ, Marshall J, Esmen NA, Borrazzo JE, Davidson CI, Small MJ, andWilkes C. 1990b. Exposure to volatile chemicals from indoor uses of water. pg 300-311 In:Total Exposure Assessment Methodology: A new horizon. Proceedings of the EPA/A&WMASpecialty Conference, Las Vegas, Nevada, November, 1989, Air & Waste ManagementAssociation, Pittsburg, PA,1990.

ATSDR 1997. Toxicological Profile for Vinyl Chloride (Update). Atlanta, Georgia: U.S.Department of Health and Human Services, Public Health Service, Agency for Toxic Substancesand Disease Registry. September 1997.

EPA 1989. Exposure Factors Handbook. Washington: U.S. Environmental Protection Agency. National Center for Environmental Research. EPA/600/8-89/043.

Jo WK, Weisel CP, and Lioy PJ. 1988. Routes of Chloroform Exposure and Body Burden fromShowering with Chlorinated Tap Water. Risk Analysis. 10(4) 575-580.

Kerger B, and Paustenbach D. 2000. Exposure to 1,1,1-TCE Vapors in a Home Due toContaminated Groundwater." Risk Anal. in press.

Kezic S, Mahieu K, Monster AC, de Wolff FA. 1997. Dermal Absorption of Vaporous andLiquid 2-Methoxyethanol and 2-Ethoxyethanol in Volunteers." Occup. Environ. Med. 54:38-43.

Mattie DR, Bates GD Jr., Jepson GW, Fisher JW, McDougal JN. 1994. Determination of Skin-Air Partition Coefficients for Volatile Chemicals: Experimental Method and Applications.Fundam. Appl. Toxicol. 22:51.

Williams PRD, Scott PK, Sheehan PJ, and Paustenbach DJ. 2000. A Probabilistic Assessment ofHousehold Exposures to MTBE in California Drinking Water. Human and Ecological RiskAssessment. 6(5): 827-849.


APPENDIX E: ATSDR RESPONSES TO HEALTH CARE QUESTIONS

The following health care programs are available to Myrtle Grove residents.

  1. The Louisiana Department of Health and Hospitals (LDHH) offers the following services:
    1. Medical assistance to current and former residents of Myrtle Grove. This would includean initial physical examination of persons with health problems found to be a result of the exposure.
    2. Medical training for local physicians on chemical exposures.
    3. Assistance in accessing health care coverage such as Medicaid and the Louisiana ChildHealth Insurance Plan.
    4. Information for residents about other programs and services of the Office of PublicHealth.


  2. The Health Resources and Services Administration (HRSA), under the U.S. Department ofHealth and Human Services, offers the following services.
    1. A health care facility in Appaloosa, Louisiana, that provides primary health care services to Louisiana residents with incomes 200% below the poverty level. Service is provided on a sliding scale based on income.
    2. A Louisiana Child Health Insurance Plan (LaCHIP) that allows for children to receiveprimary medical care if their parents have incomes 200% below the poverty level and areenrolled in the plan. The point of contact for the program is Lisa Tonrey, 214-767-0405.
    3. Health provider education. All primary care providers and nurses in Louisiana wereinvited to attend an environmental health care symposium sponsored by HRSA at LakeCharles, Louisiana, on February 23, 2002.


  3. The Southwest Center for Pediatric Environmental Health (known as the PED Unit) islocated at the University of Texas Health Center in Tyler, Texas. The address is 11937 USHighway 271, Tyler, Texas 75708-3154. This unit is the closest in relation to the MGTP.They can provide backup support to the medical community. Specifically, this unit providestelephone consultations to health care professionals. Private pediatricians, family practicephysicians, or nursing professionals who are providing health care to children of MyrtleGrove residents can contact the PED Unit in Tyler free of charge at 1-888-901-5665. Theirweb address is http://research.uthct.edu/swcpeh/.

APPENDIX F: CHEMICAL MIXTURES

Since the individual contaminants detected at the Myrtle Grove site are present at levels that arebelow levels that might be expected to result in adverse health effects, ATSDR considers that thecombined effect of all these contaminants is also not likely to be of public health concern.

This conclusion is based on studies which suggest that a mixture does not producenoncarcinogenic adverse health effects in dosed animals when the components of that mixtureare present at levels below their respective no-observed-adverse-effect levels (NOAELs), i.e., atconcentrations that would have produced no adverse effects in animals treated separately with theindividual chemicals (Feron et al. 1993; Jonker et al. 1993a; Jonker et al. 1993b; Jonker et al.1990; Groton et al. 1991). In two of these experiments (Jonker et al., 1993a, b), all of thecomponent chemicals affected the same target organ, but through different mechanisms. In twoothers (Jonker et al. 1990; Groton et al. 1991), the chemicals had different target organs andexhibited different modes of action, as do most chemicals in typical environmental mixtures.Subsequent experiments have shown similar results (Feron et al. 1995; Groton et al. 1997).

Notwithstanding the conservative regulatory policy assumption of zero-threshold forcarcinogens, carcinogens do exhibit practical thresholds in the laboratory, no less than dononcarcinogens (SOT 1981; Williams and Weisbuirger 1991; Cunningham 1994). Thus, it is notunlikely that the principle described in the previous paragraph will be applicable to carcinogens,as well as to noncarcinogens. Animal evidence supports this surmise. When Hasegawa et al.(1994) administered 10 carcinogenic heterocyclic amines in combination to rats at 1/100 of thedoses known to be carcinogenic individually, the effects did not differ significantly fromcontrols. These doses were 100 times lower than established cancer effect levels. Environmentallevels of exposure that humans encounter are typically much lower, still, by many orders ofmagnitude. These results suggest that mixed exposures to carcinogens below all known effectslevels are unlikely to pose any realistic carcinogenic risk to exposed humans.

The aforementioned research findings support the conclusion that because the individualcontaminants detected at this site were present at levels well below those that might be expectedto produce cancerous or noncancerous adverse health effects, the combined effect of all thesecontaminants is also unlikely to be of public health concern.

References and Documents Reviewed

Cunningham ML, Elwell MR, and Matthews HB. 1994. Relationship of carcinogenicity andcellular proliferation induced by mutagenic noncarcinogens vs carcinogens. Fundamental andApplied Toxicology, 23: 363-369.

Feron VJ, Jonker D, Groten JP, Horbach GJMJ, Cassee FR, Schoen ED, Opdam JJG. 1993. Combination technology: From challenge to reality. Toxicology Tribune 14: 1-3.

Feron VJ, Groten JP, van Zirge JA, Cassee FR, Jonker D, and van Bladeren PJ. 1995. Toxicitystudies in rats of simple mixtures of chemicals with the same or different target organs. Toxicology Letters 82-83: 505-512.

Groton JP, Sinkeldam EJ, Luten JB, van Bladeren PJ. 1991. Interaction of dietary calcium,potassium, magnesium, manganese, copper, iron, zinc, and selenium with the accumulation andoral toxicity of cadmium in rats. Food and Chemical Toxicology 4: 249-258.

Groten JP, Schoen ED, van Bladeren PJ, Kuper CF, van Zorge JA, and Feron VJ. 1997. Subacute toxicity of a mixture of nine chemicals in rats: detecting interactive effects with afractionated two-level factorial design. Fundamental and Applied Toxicology 36: 15-29.

Hasegawa R, Miyata E, Futakuchi M, Hagiwara A, Nagao M, Sugimura T and Ito N. 1994. Synergistic enhancement of hepatic foci development by combined treatment of rats with 10heterocyclic amines at low doses. Carcinogenesis 15: 1037-1041.

Jonker D, Woutersen RA, van Bladeren PJ, Til HP, Feron VJ. 1990. 4-week oral toxicity studyof a combination of eight chemicals in rats: comparison with the toxicity of the individualcompounds: Food and Chemical Toxicology; 28: 623-631.

Jonker D, Jones MA, van Bladeren PJ, Woutersen RA, Til HP, Feron VJ. 1993a. Acute 24 hourtoxicity of a combination of four nephrotoxicants in rats compared with the toxicity of theindividual compounds. Food and Chemical Toxicology 1993; 31: 45-52.

Jonker D, Woutersen RA, van Bladeren PJ, Til HP, Feron VJ. 1993b. Subacute (4-wk) oraltoxicity of a combination of four nephrotoxicants in rats: comparison with the toxicity of theindividual compounds. Food and Chemical Toxicology 31: 45-52.

SOT 1981. Society of Toxicology. Re-evaluation of the ED01 Study. Fundamental andApplied Toxicology 1:27-128.

Takayama S, Hasagawa H and Ohgaki O. 1989. Combination effects of forty carcinogensadministered at low doses to male rats. Jpn. J. Cancer Res. 80: 732-736.

Williams GM, and Weisburger JH. 1991. Chemical Carcinogenesis. Chapter 5 in: Casarett andDoull's TOXICOLOGY: The Basic Science of Poisons. (Mary O Amdur, John Doull, and CurtisKlaassen, Editors.) Pergamon Press, pp. 127-200.


1. The term "gavage" refers to the administration of a test substance directly into the animal's stomach via a tube inserted down its throat. Because rats cannot vomit, this practice enables investigators to know exactly how much of the substance the animals received.


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