october 12th, 2005 mr. john leahy, senior advisor · mr. john leahy, senior advisor special review...

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Networking Council

David BennettCanadian Labour Congress

Neva HassaneinUniversity of MontanaEnvironmental Studies Program

Rod MacRaeFood Policy Consulting

Janet MayToronto Environmental Alliance

Tirso MorenoThe Farmworker Associationof Florida, Inc.

Claudio Torres NachónCentro de Derecho Ambiental eIntegración Económica del Sur

Sharyle PattonCommonweal Health andEnvironment Program

Anna María Ruiz DíasRed de Permacultura México

Bryony SchwanWomen’s Voices for the Earth

Lucy SharrattPolaris Institute

Gregg SmallWashington Toxics Coalition

Board of Directors

Rajiv BhatiaRichard BunceIgnacio H. ChapelaSandra “JD” DolinerMartha HerbertMaría Elena Martínez-TorresMichelle MascarenhasJosé R. PadillaMichael PickerPatricia ScottAmy C. ShannonKay Treakle

Co-Directors

Monica MooreStephen Scholl-Buckwald

October 12th, 2005

Re: Comments on the Fumigant Cluster Assessment

Mr. John Leahy, Senior AdvisorSpecial Review and Reregistration Division (7508C)Office of Pesticide ProgramsEnvironmental Protection Agency1200 Pennsylvania Av NWWashington, DC 20460-0001

Dear Mr. Leahy:

This letter and the attachment that follows are a submission to dockets:

Methyl Bromide Risk Assessment, OPP-2005-01231,3-Dichloropropene Risk Assessment, OPP-2005-0124Metam Sodium Risk Assessment, OPP-2005-0125Dazomet Risk Assessment, OPP-2005-0128

In what follows, we will refer to these concurrent risk assessments as well as theexpected forthcoming fumigant risk assessments as the “Fumigant ClusterAssessment,” and to the Technical Briefing on July 13th that covered the FumigantCluster Assessment as the “Technical Briefing.”

We thank the Environmental Protection Agency (EPA) staff for the TechnicalBriefing, which provided a detailed orientation to the entire fumigants clusterassessment process, science and analysis. We also thank the EPA for this opportunityto comment on this phase of the Fumigant Cluster Assessment.

Our comments fall into the following areas:

1. Risk Assessment Methodology, General2. Bystander Exposure Assessment3. Occupational Exposure Assessment4. Methyl Bromide Toxicology5. 1,3-Dichloropropene Toxicology6. Metam Sodium and Dazomet Toxicology7. Fumigant Usage, Need, and Alternatives

Many of these areas (1, 2, 3, and 7) are applicable to every fumigant in the FumigantCluster Assessment. Only areas 4, 5 and 6 are specific to particular fumigants. Eacharea has a corresponding section in the attachment that follows.

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Because of the diversity of expertise required to write each section, the sections have separateleads. The lead author for Sections 1 and 4 is Michael J. DiBartolomeis, PhD, DABT, ConsultingToxicologist, Pesticide Action Network, North America (PANNA). For Section 2, Brian R. Hill,PhD, Staff Scientist, PANNA. For Sections 3 and 6 Anne Katten, MPH, Pesticide and WorkSafety Specialist, California Rural Legal Assistance Foundation (CRLAF). For Section 5, SusanE. Kegley, PhD, Senior Scientist, PANNA. For Section 7, Katherine Mills, Assistant Scientist,PANNA. Questions or requests for clarifications can be directed to the respective section leadsvia PANNA, (415) 981-1771, and CRLAF, (916) 446-7904.

What follows are highlights of the respective sections:

Risk Assessment Methodology, General

a. Overall, there is a lack of clarity and detail provided in the risk assessment documentswith respect to toxicology, dose-response assessment, and the scientific support for theconclusions and assumptions made. We offer specific recommendations in our commentsto improve the information and results presented in the US Environmental ProtectionAgency’s (US EPA’s) risk assessments.

b. Although we do not object to the use of pharmacokinetic data to refine the fumigant riskassessments, we do believe that the scientific support and information provided in USEPA’s calculation of human equivalency concentrations (HEC) in each risk assessment isinadequate. Another flaw in the US EPA’s derivation of HECs is that test animalexposures to fumigants do not match typical human exposures. We offer specificrecommendations in our comments to make the derivation of HECs for inhalationexposures more transparent and accurate.

c. In general, the discussion and justification for the use of uncertainty factors in the riskassessment is difficult to follow, and the rationale for selecting uncertainty factorsunclear; it appears to us that US EPA’s decisions were subjective and arbitrary. Werecommend that US EPA adopt the more widely used default methodology, as explainedin our comments, and consider additional uncertainty factor applications in specific cases.

d. In general, the sections referring to aggregate risk in the risk assessments are toosuperficial to fully understand what US EPA is attempting to do. We recommend that USEPA revise the risk assessment documents to include a full quantitative analysis for thecombination of the three major exposure routes for all exposure sources for eachchemical fumigant.

e. There is no attempt by US EPA to consider human exposures to mixtures of fumigants, orsequential exposures to the fumigants as they are applied in practice. We provide specificexamples in our comments on how the risk assessments could be revised to includecumulative risk assessment.

f. In conducting cumulative risk assessments, we urge US EPA to define the methodologyin broader terms than simply summing the risks for comparable toxicity endpoints forchemicals with the same mechanism of action. Detrimental effects to the body caused bya chemical might make an individual more vulnerable to the toxicity of another chemical,which acts by a different mechanism. In the absence of data to substantiate taking noaction, an additional uncertainty factor is indicated.

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Bystander Exposure Assessment

a. A review of major poisonings shows that common features are low wind speeds and otherconditions necessary for high atmospheric stability.

b. Low wind speeds occur frequently, during at least 10% of the hours annually, and up to30% of the hours depending on the cutoff defining low wind speeds and the weatherstations used for the estimates.

c. The ISCST3 model and methodology used by EPA systematically underestimates airconcentrations during calm and near-calm wind conditions by treating concentrationscalculated for these conditions as missing.

d. The AERMOD model which can provide estimates under these circumstances isavailable and should be used to compute realistic fumigant air concentrations.

e. Use of the AERMOD model instead of the ISCST3 model in this circumstance is incompliance with EPA regulatory guidelines.

f. There is insufficient detail to follow or comment on the indirect back-calculation methodfor determining flux. Detail lacking includes the field monitoring studies used, the criteriafor combining or eliminating study results, and the comparison of study results. The fluxcalculation and hence the exposure modeling calculation are therefore not transparent.

g. The model (including its calibration through the back-calculation of flux values) was notcorroborated with known major poisoning incidents. Demonstrating that the calibratedmodel correctly predicts past incidents would increase confidence that the model resultswill correctly validate risk mitigation strategies and prevent future incidents.

h. Dismissal of ambient chronic and sub-chronic exposure is premature for multiple reasonsincluding the fact that some of the existing studies did indicate that levels of concernwere exceeded, the sensitivity of the result to HEC and MOE values, and trends ofincreasing use which render old air monitoring studies obsolete.

i. Assessments for multiple (successive, geographically neighboring) applications have notbeen included and will increase the exposure estimates when they are.

Occupational Exposure Assessment

a. These risk assessments show that a majority of occupational exposures to metam sodium,dazomet and methyl bromide are much too high, with the Agency’s estimates of exposurefor many jobs having little or no safety margin.

b. Our concerns are heightened because these risk assessments are based on manyassumptions which underestimate occupational exposures. Specifically we conclude thatthe length of workday, number of days worked per year and fumigant exposure levels areunderestimated.

c. In contrast, respiratory protection factors are overestimated.

Methyl Bromide Toxicology

a. The selection of the toxicity endpoints for acute methyl bromide toxicity from inhalationor dietary exposure is adequately supported by the data and the studies available to USEPA.

b. We do not agree with the choice of study and dose selection for the assessment of“short-term” and “intermediate” methyl bromide exposure and human health risks. Asexplained in our comments, we conclude that an estimated no-observed-adverse-effectlevel (NOAEL) of 0.5 ppm (0.14 mg/kg-day) should be used for assessing short-term andintermediate risk of methyl bromide exposure. US EPA arrived at the same conclusion in2003. However, in its 2005 document, US EPA changed its conclusions to weaken the

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standard without any explanation. This is a key issue for methyl bromide risk assessmentas it is the primary determinant whether methyl bromide can continue to be used inagricultural fields in and around residential areas.

c. To assess the risk of chronic inhalation toxicity, we recommend using the basal cellhyperplasia toxicity endpoint in rats (LOAEL = 3 ppm) as used by US EPA, but with anadditional uncertainty factor of ten to account for uncertainties as explained in ourcomments.

d. We recommend that the more health-protective toxicity endpoint and dose level ofconcern (1.5 ppm) from a chronic dog study be used in the dietary exposure riskassessment rather than the NOAEL of 50 ppm from a rat study.

e. US EPA needs to include an estimate of the risks from dermal exposure to methylbromide alone and in combination (aggregate) with other exposures.

f. Due to the uncertainties associated with the differential toxicity findings betweendeveloping and adult animals, case reports of human exposures, and the geneticpolymorphisms that exist for the metabolism of methyl bromide, we conclude that anadditional uncertainty factor of ten be used in calculating the target concentrations in air,water, and the diet for methyl bromide that are fully protective of infants and children.

g. Chloropicrin is combined with methyl bromide as a warning agent and also as an activeingredient. Therefore, it is essential that US EPA quantify the health risks of the exposureto the combination of methyl bromide and chloropicrin, including a completetoxicological evaluation of combined toxicity, exposure, and interaction betweenchloropicrin and methyl bromide to address the risk of using these the formulations.

1,3-Dichloropropene Toxicology

a. We have serious concerns about the use of the Human Equivalent Concentration (HEC)methodology to estimate human No Observed Adverse Effect Level (NOAEL) values for1,3-D. The documentation provided does not provide any scientific justification for thechoice of an uncertainty factor of three instead of ten.

b. The acute NOAEL of 454 ppm selected by EPA is too high. We recommend that 10 ppmbe used as the more health-protective critical endpoint for acute toxicity, using the valuefrom the dominant lethal assay (for inhalation in rat). Few details about this study areprovided by EPA. We request that EPA provide a description for this study and anexplanation for why this NOAEL was not used as the critical endpoint for acute toxicity.Our recommendation on the use of this study may change if EPA provides the requestedadditional information.

c. The subchronic HEC of 5.0 ppm selected by EPA is too high. The critical endpoint forsubchronic toxicity should be 2.5 ppm, as taken from the rabbit study. We recommendthat 2.5 ppm be used as the more health-protective critical endpoint for subchronictoxicity.

d. Chloropicrin is combined with 1,3-D as a warning agent and also as an active ingredient.Therefore, it is essential that US EPA quantify the health risks of exposure to thecombination of 1,3-D and chloropicrin, including a complete toxicological evaluation ofcombined toxicity, exposure, and potential interactions between chloropicrin and 1,3-D toaddress the risk of using these the formulations.

e. EPA underestimates the cancer risks from use of 1,3-D. The only data that are availableto assess this risk are from California Air Resources Board (CARB) monitoring.California has strict township caps and other use limitations on 1,3-D. Thus these data tonot provide accurate exposure estimates for other states, and underestimate exposure inthe highest use areas.

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f. Use of this fumigant has increased since these studies were conducted, from 4.0 millionpounds in 2001 to 7.0 million pounds in 2003. Additionally, the monitoring studies onwhich EPA is basing their conclusions were conducted in counties where 1,3-D use is notthe highest in California.

g. All of these factors contribute to a substantial under-estimation of cancer risks.h. The metabolism section of this report contains subjective and non-scientific language and

terminology, and no quantitative information is provided. Without the numbers andcomplete descriptions of metabolites to fully characterize the effects and time frame ofthe pharmacology, these study descriptions are of virtually no scientific value.

i. US EPA needs to include an estimate of the risks from dermal exposure to 1,3-D aloneand in combination (aggregate) with other exposures.

Metam Sodium/Dazomet Toxicology

a. Our analysis revealed that several toxicology endpoints utilized for metam sodium andMITC are not as health protective as those adopted by California DPR. The Agency has,in contrast, harmonized with DPR on a more health protective MITC acute inhalationeffect level, but we conclude an additional uncertainty factor is warranted to assureprotection of sensitive populations.

b. A Food Quality Protection Act factor should be reconsidered given the well-documentedexposure of children to MITC in ambient air and the existing data gaps.

c. Exposure of workers and the general public to other breakdown products of metamsodium and dazomet are also of concern, and the risk assessments should evaluatecumulative exposure impacts. These breakdown products include methyl isocyanate,hydrogen sulfide, carbon disulfide, methylamine and formaldehyde.

d. Finally, we are extremely concerned about the numerous MITC toxicology data gaps andurge the Agency to request initiation of studies to fill these data gaps without furtherdelay and consider suspension of use in the interim.

EPA Must Seriously Consider Existing Viable Alternatives

a. The substantial evidence of the hazards fumigants pose to workers and bystandersindicates that EPA cannot be assured that there is a reasonable certainty of no harm fromregistration and use of these chemicals. For workers especially, it is clear that the extremerisks outweigh the limited benefits.

b. The fumigants considered in this cluster assessment have viable non-toxic alternativesthat are being used successfully for fumigant-intensive crops in many climatic andecological zones. These fumigants continue to be responsible for mass poisonings as wellas chronic adverse health effects. We urge EPA to invest more resources in alternativesassessment work with USDA to help farmers transition away from fumigants as a soilpest control strategy.

These are merely representative highlights illustrating the range of issues covered in theattachment that follows. Please consult the attachment for details.

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We thank EPA staff in advance for studying our comments and addressing the areas discussedduring subsequent phases of the Fumigant Cluster Assessment.

Sincerely,

Susan E. Kegley, PhD, Senior Scientist, PANNA

Brian R. Hill, PhD, Staff Scientist, PANNA

Michael J. DiBartolomeis, PhD, DABT, Consulting Toxicologist, PANNA

Katherine Mills, Assistant Scientist, PANNA

Anne Katten, MPH, Pesticide and Work Safety Specialist, CRLAF

Cosigned,

Shelley Davis, Co-Executive Director, Farm Worker Justice Fund

Michael Green, Executive Director, Center for Environmental Health

Norma Grier, Director, Northwest Coalition for Alternatives to Pesticides

Bill Walker, Vice President/West Coast, Environmental Working Group and EWG Action Fund

Carol Dansereau, Executive Director, Farm Worker Pesticide Project

Fawn Pattison, Executive Director, Agricultural Resources Center & Pesticide Education Project

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Comments on the Fumigant Cluster Assessment

1 Risk Assessment Methodology, General ..................................................................................... 91.1 Toxicology Assessment....................................................................................................... 91.2 Derivation of Human Equivalent Concentrations............................................................. 111.3 Uncertainty Factors............................................................................................................ 121.4 Aggregate Risks................................................................................................................. 131.5 Cumulative Risk ................................................................................................................ 13

2 Bystander Exposure Assessment................................................................................................ 152.1 Air Model ........................................................................................................................... 15

2.1.1 Introduction............................................................................................................... 152.1.2 Recent Major Poisonings.......................................................................................... 152.1.3 Relative Frequency of Low Wind Conditions ......................................................... 182.1.4 Evidence for High Atmospheric Stability Classes .................................................. 212.1.5 Additional Evidence for the Importance of High Atmospheric Stability Classes.. 222.1.6 Adequacy of PERFUM/ISCST3 .............................................................................. 232.1.7 EPA Recommendations on Alternative Models ...................................................... 242.1.8 Air Modeling Conclusions ....................................................................................... 26

2.2 Other Exposure Modeling Considerations........................................................................ 262.2.1 Comparison of Exposure Modeling Methodologies................................................ 262.2.2 Model Calibration, Flux Estimates .......................................................................... 262.2.3 Corroboration of Calibrated Model with Actual Incidents ..................................... 272.2.4 Use of Maximum vs. Whole Field Method ............................................................. 282.2.5 Consideration of Exposure from Multiple Field Fumigations in the SameGeographic Area and Time Period............................................................................................. 282.2.6 Dismissal of Ambient Exposure............................................................................... 28

3 Occupational Exposure Analysis................................................................................................ 293.1 Number of Workdays ........................................................................................................ 293.2 Length of Workday............................................................................................................ 293.3 Dermal and Ocular Exposure ............................................................................................ 293.4 Respiratory Protection Factors .......................................................................................... 303.5 Respirator Cartridges and Canisters.................................................................................. 30

3.5.1 Respirator Cartridges and Canisters for Methyl Bromide....................................... 303.5.2 No Explanation for Protection Factors Assigned to Engineering Controls............ 313.5.3 No Consideration of Heat Stress Prevention ........................................................... 31

4 Methyl Bromide Toxicology ...................................................................................................... 324.1 Selection of Critical Toxicity Study Endpoints for Risk Assessment ............................. 32

4.1.1 Acute Toxicity .......................................................................................................... 324.1.2 Subchronic (Intermediate) Toxicity ......................................................................... 324.1.3 Chronic Toxicity....................................................................................................... 34

4.2 Toxicology Data Gaps ....................................................................................................... 344.3 Dermal Exposure Risk Assessment .................................................................................. 344.4 Uncertainty Factors............................................................................................................ 35

4.4.1 General ...................................................................................................................... 354.4.2 Further Protection of Infants and Children .............................................................. 35


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4.4.3 Chronic Toxicity Uncertainty Factor ....................................................................... 384.4.4 Carcinogenicity......................................................................................................... 38

4.5 Cumulative Risk Assessment: Chloropicrin Plus Methyl Bromide................................. 394.6 Aggregate Risk Assessment .............................................................................................. 40

5 1,3-Dichloropropene Toxicology ............................................................................................... 415.1 Use of Human Equivalent Concentration Methodology .................................................. 415.2 Selection of Critical Toxicity Study Endpoints for Risk Assessment ............................. 41

5.2.1 Acute Toxicity .......................................................................................................... 415.2.2 Developmental Toxicity ........................................................................................... 425.2.3 Subchronic (Intermediate) Toxicity ......................................................................... 425.2.4 Carcinogenicity......................................................................................................... 42

5.3 Metabolism Studies ........................................................................................................... 435.4 Dermal Exposure Risk Assessment .................................................................................. 445.5 Uncertainty Factors............................................................................................................ 445.6 Cumulative Risk Assessment: 1,3-D Plus Chloropicrin................................................... 455.7 Aggregate Risk Assessment .............................................................................................. 45

6 Metam Sodium and Dazomet Toxicology ................................................................................. 466.1 Choice of NOAELs............................................................................................................ 46

6.1.1 Metam Short-Term Dermal NOAEL ....................................................................... 466.1.2 MITC Short and Intermediate-Term Effect Level................................................... 466.1.3 MITC Acute Inhalation Effect Level ....................................................................... 466.1.4 Limitations of Acute Inhalation Toxicity Studies for MITC .................................. 47

6.2 Use of Uncertainty Factors/FQPA Factor/MOEs............................................................. 496.2.1 FQPA Factor ............................................................................................................. 49

6.3 Additional Issues................................................................................................................ 496.3.1 Failure to Consider Cumulative Exposure to other Degradation Products............. 496.3.2 Metam Sodium Field Monitoring Should Not Require Chemical Inhalation......... 506.3.3 MITC and Dazomet Data Gaps Are Alarming ........................................................ 506.3.4 Summary does not Accurately Characterize Metam Sodium Illness Reports........ 506.3.5 Metam Sodium (MITC) Monitoring Studies Underestimate Bystander Exposure

507 US EPA Must Seriously Consider Existing Viable Alternatives.............................................. 53

7.1 Percentage of Crops Treated with Soil Fumigants ........................................................... 537.2 US EPA Must Consider the External Costs of Fumigant Use ......................................... 547.3 Fumigant-Intensive Crops Can Be Grown Cost Effectively without Soil Fumigants..... 55

7.3.1 Strawberries and Tomatoes ...................................................................................... 557.3.2 Potatoes and Carrots ................................................................................................. 56

Endnotes ............................................................................................................................................... 58

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1 Risk Assessment Methodology, General

1.1 Toxicology AssessmentOverall, there is a lack of clarity and detail provided in the risk assessment documents withrespect to toxicology, dose-response assessment, and the scientific support for the conclusionsand assumptions made. In short, a much more comprehensive summary of registrant toxicity testswith detailed descriptions of test results must be provided by US EPA to enable the public toevaluate the validity of the risk assessment. For the most part, the sections in US EPA’s riskassessments devoted to toxicity and toxicology profiles are incomplete and often containsubjective and non-scientific language and terminology. For example, terms like “marginal,” or“less severe” are used to describe toxicological effects. These terms, without a quantitativeranking system or comparative scale, are of virtually no scientific value. In addition, there is oftenno statistical analysis of the data presented and no quantitative determination of statisticalsignificance included in these toxicology summaries. Validation of the selected no-observed-adverse-effect levels (NOAELs) and lowest-observed-adverse-effect levels (LOAELs) cannot bemade without this key information. Furthermore, in most cases, numbers of animals in the testgroups are not provided in the toxicology section, nor are test-animal mortality rates forsubchronic, chronic, and cancer studies, making it difficult to accurately assess the toxicity of thesubstance being tested.

At a minimum, the following information should be provided for every toxicological studysummary:

a) Experimental doses used in both units of concentration (e.g., ppm) and dose per bodyweight (e.g., mg/kg-day).

b) Number of animals per dose group.c) The exact duration and frequency of exposures.d) Purity of active ingredient tested and identity of any impurities.e) List of endpoints evaluated (whether positive results, or not).f) Observations of animal appearance and behavior after exposure and numbers of

animals affected.g) Observations of pathological histological results and numbers of animals affected.h) The time elapsed between exposure and assessment of potential adverse effects.i) Number of animals that died or were sacrificed during the test period.j) Statistical comparisons of dose-related toxicological effects.

The California Department of Pesticide Regulation (CDPR) routinely includes in its riskassessments and Toxicology Data Review Summaries1 more complete descriptions of eachtoxicology study submitted by the registrant, including a complete description of the experimentaldesign and statistical analyses of the data. Where applicable, publications obtained in the peer-reviewed literature are used to supplement the registrant’s database. We request that US EPAreview the relevant CDPR documents for each fumigant and include comparable levels of detailand scientific analysis in its revised risk assessment documents and present more scientificallybased text in the revised risk assessment. We also recommend that US EPA identify and


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summarize areas of scientific disagreement with CDPR so that differences in interpretation andmethodology are transparent, readily understood, and open for public scrutiny. Some examples ofsuch scientific disagreement are provided in the chemical-specific comments.

In general, the information presented on the toxicology of each fumigant is limited to studiesselected from the data submitted by the registrants to satisfy registration requirements. Studies notused by US EPA are not included in the toxicology summaries. Nevertheless, without a summaryof the complete database, it is not possible to validate the selections made by US EPA nor is itpossible to make a determination regarding the overall weight-of-evidence for a given fumigant.Because the data submitted by registrants is not generally publicly available, we request that USEPA expand the toxicology sections to include summaries of all of the data submitted by theregistrants for each fumigant, whether they are guideline studies or not. Alternatively, US EPAmight consider attaching CDPR’s toxicology summaries as an appendix. Although there stillcould be improvement in CDPR’s documentation summarizing key studies, the informationpresented in CDPR’s documents is more complete than what US EPA provides in its riskassessments. This alternative would also facilitate comparing US EPA and CDPR’sinterpretations of the same scientific data.

It is not clear whether US EPA also searched the published literature for additional experimentalor epidemiological studies for use in risk assessment, but it is apparent that if this were the case,US EPA did not consider those studies in its toxicity assessments. According to the Office ofManagement and Budget2, “in the 1996 amendments to the Safe Drinking Water Act, Congressadopted a basic quality standard for the dissemination of public information about risks ofadverse health effects. Under 42 USC 300g-1(b)(3)(B), the agency [US EPA] is directed, ‘toensure that the presentation of information [risk] effects is comprehensive, informative, andunderstandable.’ The agency is further directed, ‘in a document made available to the public insupport of a regulation [to] specify, to the extent practicable - … (v) peer-reviewed studies knownto the [agency] that support, are directly relevant to, or fail to support any estimate of [risk]effects and the methodology used to reconcile inconsistencies in the scientific data.’ ” Althoughthese instructions were directed to a different program in US EPA, for consistency reasons andfor thoroughness, we recommend that for all of the fumigants considered in the fumigant cluster,US EPA conduct a comprehensive search of the peer-reviewed literature and governmentdocuments for studies on toxicology, epidemiology, metabolism and other pharmacokinetic data,environmental fate, and risk assessment. We believe that important information available in thepeer-reviewed literature is neither included nor addressed in the registrants’ applications forregistration At a minimum, US EPA should include in its risk assessments citations andreferences to the studies found as a result of a comprehensive literature search, and if notsummarized and considered in the toxicity assessment, an explanation as to why the study resultswere rejected.

It would be helpful for comparative purposes if the toxicity endpoints for key studies and thecorresponding doses for each fumigant were combined into one table and discussed in terms ofcommon as well as unique toxicity endpoints. Currently, the toxicology sections in the riskassessments for each fumigant are individualized, with no cross-chemical discussion. If USEPA’s intent were to actually consider the fumigants as a cluster or a family of chemicals, then acomparative assessment of the toxicity and levels of concern would need to be included to helpdetermine relative hazards of each fumigant.


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1.2 Derivation of Human Equivalent ConcentrationsUS EPA states in its risk assessment that the methodology used to estimate human doses ofinhaled chemicals from experiments in animals differs from CDPR’s method. The bottom line,however, is that the most significant difference between US EPA’s methodology and the standarddefault methodology used by CDFA and other risk assessors is that US EPA routinely attempts toincorporate pharmacokinetic considerations in its calculations, regardless of the lack of quality ofthe available data. The desire to refine risk assessments by utilizing species- and chemical-specific data describing how physiological factors that might affect chemical toxicity is not a newconcept. However, chemical-specific phamacokinetic data is often limited and the results of usingpharmacokinetic models are often not validated with empirical data, nor are the modelingassumptions made readily available to the public.

Although we do not object in principle to the use of pharmacokinetic data to refine the fumigantrisk assessments, we do believe that the scientific support and information provided in US EPA’shuman equivalency section in each risk assessment is inadequate. In US EPA’s 2002 TechnicalPanel Review of the RfC and RfD Processes, US EPA itself indicated that “. . . constructing aPBPK model is an information-intensive process that requires much chemical-specific data,including route-specific data. Such sophisticated data and models are available usually for only asubset of chemicals that have extensive databases.”3 Although the methods are briefly discussed,the data and level of detail provided for each fumigant is not sufficient to allow the results to beconfirmed. No data are presented to justify reduction of the interspecies uncertainty factor fromten to three. If US EPA believes that most of the interspecies differences arise frompharmacokinetic effects instead of pharmacodynamic effects, data must be presented that justifythat conclusion. We suspect however, that chemical-specific pharmacokinetic andpharmacodynamic data are not available and that US EPA has resorted to using generalassumptions about chemical fumigants that may or may not be accurate. If the goal is to refine therisk assessment methods and results, then it must obtain data to achieve that purpose.

Another flaw in the HEC process is that test animal exposures to fumigants do not match typicalhuman exposures. Most inhalation studies on laboratory animals are at a constant concentrationfor six to eight hours per day, five days per week, providing ample time for the animals’ repairsystems to respond to the chemical insult during the “rest” periods. Exposure patterns for peopleliving near fumigant application sites are substantially different, with an exposure spike that mayeven have acute effects occurring during the first day or two after the application, followed by adecreasing concentration over the next week or so. Exposure can be continuous (assuming onestays at home and the wind direction is constant), with no opportunity for recovery. Because ofthe possibility of mixed acute and subchronic effects, this failure in inhalation exposure testing islikely to be one of the most significant flaws in current reference concentration (RfC)methodology that leads to an underestimation of the actual HEC.

Additionally, documents essential to the complete understanding of the methodology cited inAppendix B for the fumigant risk assessments, were not made available as part of the riskassessment documents, nor were they even properly referenced. For example, in the secondparagraph of Appendix B, the second sentence begins “Based on the RfC guidance (1994), themethodology for RfCs . . .” and in a later paragraph “The MVanimal is calculated using theallometric scaling provide in US EPA (1988a)” A look at the end of the document indicates thatno references are listed, making it impossible to even determine which of US EPA’s thousands ofdocuments are being cited. The one document with a listed title, “Methods for Derivation ofInhalation Reference Concentrations and Application of Inhalation Dosimetry (1994)” is not


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readily available for download from US EPA’s Web site and US EPA’s 2002 guidance documenton RfC methodology is not referenced at all.

In order to make the derivation of HECs for inhalation exposures more transparent, werecommend that US EPA do the following:

a) Revise the appendix on the derivation of HECs for each chemical fumigant to includea summary of the chemical-specific pharmacokinetic data available. The data shouldbe obtained from the registrant’s file as well as the peer-reviewed scientific literatureand other available sources of scientific data and analysis. The burden should beplaced on US EPA to present sufficient scientific documentation to confirm that theuse of its methods is actually more refined and reliable than the standard defaultmethods.

b) Include a side-by-side comparison of the risk results obtained when incorporatingpharmacokinetic data and the lower uncertainty factors with the standardmethodology and the higher uncertainty factor.

c) Show the actual calculation used for each critical endpoint in the risk assessmentdocument. Include the specific variables used in the calculation, cite the sources andinclude units.

d) Include full citations to all referenced documents, including specific links to websites where the documents can be downloaded (or add the documents to the E-Docket).

e) Because animal inhalation studies do not effectively mimic human exposures, USEPA should increase the value of the uncertainty factor to ensure that the HEC is notan underestimate of human exposure.

In most cases, we suspect that the adjusted concentrations will be very similar regardless of themethod used. If this is the case for the fumigants, it might be best to reach agreement with CDPRon one methodology to apply to pesticide risk assessments in order to avoid the difficulty incomparing results. Both CDPR and US EPA would need to achieve the same standard of proofthat the deviation from default methodology actually produces a more reliable and accurate riskassessment, particularly as it relates to dose extrapolation across species.

1.3 Uncertainty FactorsIn general, the discussion and justification for the use of uncertainty factors in the risk assessmentis difficult to follow and the rationale for selecting uncertainty factors so unclear as to appear as ifUS EPA’s decisions were subjective and arbitrary. We recommend that US EPA adopt the morewidely used and recognized methodology in risk assessment for deriving levels of concern forhumans from toxicity data. That is, dividing NOAELs by factors of ten (or factors of three onlywhen adequate data and scientific support are available and a complete discussion provided) tocorrect for interspecies (10x) and intraspecies (10x) variation, converting LOAELs to NOAELs(3-10x), and for addressing inadequacy or uncertainty in the database (3-10x). Deviation from thedefault values should be substantiated with scientific data and a transparent analysis.

Finally, US EPA should include an additional uncertainty factor of three to ten to account forhuman error. Assumptions that pesticide users will always use personal protective equipment,always follow the label directions, and that no accidents will ever happen, are flawed. Thepoisoning incident reports (which represent only the tip of the iceberg of actual poisoningincidents) indicate that “accidents” happen frequently, as does misuse and misapplication. In


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addition, it is unrealistic to expect workers to use restrictive and hot personal protectiveequipment on 90-degree-plus days—a common occurrence during fumigant application seasonsin both California and Florida. Failing to include a “human error” uncertainty factor for fumigantuse is similar to a failure to put a traffic control device at a busy intersection at which manyaccidents have occurred. It is irresponsible of US EPA to base its risk assessments ondemonstrably faulty assumptions.

1.4 Aggregate RisksIn general, the sections referring to aggregate risk in the risk assessments are too superficial tofully understand what US EPA is attempting to do. For each fumigant there are four distinctsources of exposure in the environment and workplace (air, water, diet, and direct contact) andthree important exposure routes (inhalation, ingestion, and dermal contact). An appropriateaggregate risk assessment for a single chemical should consider all routes of exposure together tocharacterize short-term (acute), intermediate (subchronic) and long-term (chronic) risks. Commontoxicity endpoints and mechanisms of activation and toxicity need to be identified for eachchemical and each route of exposure. Pharmacokinetic data might also need to be considereddepending on how the chemical enters the body, and how it is distributed among the organs andtissues, bioactivated or detoxified, and finally excreted.

At a minimum, aggregate risks can be estimated for common toxicity endpoints shared by two ormore exposure routes. When toxicity information is lacking for one exposure route, it is notacceptable to dismiss the route of exposure as insignificant or negligible. Although not ideal,toxicity data for one exposure route might need to be extrapolated as surrogate data for anotherroute of exposure, incorporating available information regarding pharmacokinetic andpharmacodynamic differences.

We recommend that US EPA revise the risk assessment documents to include a full quantitativeanalysis of all three exposure routes and all four exposure sources for each chemical fumigant andprovide a summary table showing aggregate risks for acute, subchronic, and chronic exposure toeach fumigant. If data are not available, then an additional uncertainty factor should beincorporated into the risk results to offer greater public health protection in the absence ofadequate data.

1.5 Cumulative RiskThere is no attempt by US EPA to consider human exposures to mixtures of fumigants, orsequential exposures to the fumigants as they are applied in practice. In its May 2005 letter to USEPA, the Fumigant Users Group specifically states “Each of these fumigants plays a unique andcritical role in the crop protection system. Occasionally they are used together in end-useformulations with other active ingredients, or applied sequentially to control crop pests.”4

Therefore it is important to consider the fumigants as a category of chemicals to which residentsand workers might be exposed in mixtures or in exposure sequences reflective of their use inagriculture.

The most obvious example of chemical fumigant mixtures is the addition of chloropicrin as anodorant and/or an active ingredient in fumigant formulations. However, cumulative riskassessment should not be limited to the more common exposure scenarios, but rather becomprehensive in nature, describing quantitatively if possible the additive, synergistic, orantagonistic effects of the fumigants when used together in formulation. It is of equal importance


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to estimate the impact on human health of being exposed to the fumigants in sequence. Forexample, exposure to a respiratory irritant such as chloropicrin might result in sensitization of therespiratory tract, which in turn might sensitize an individual to asthmatic reactions when the sameindividual is exposed to methyl isothiocyanate, another respiratory irritant, at otherwise very lowair concentrations.

In conducting cumulative risk assessments, we urge US EPA to define the methodology inbroader terms than simply summing the risks for comparable toxicity endpoints for chemicalswith the same mechanism of action. Detrimental effects to the body caused by a chemical mightmake an individual more vulnerable to the toxicity of another chemical, which acts by a differentmechanism. Furthermore, sensitive and vulnerable subpopulations need to be identified forcumulative impacts that might not be predicted in the average, healthy adult population. In theabsence of data to substantiate taking no action, additional uncertainty needs to be applied to arisk assessment to account for cumulative impacts on more vulnerable populations.

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2 Bystander Exposure Assessment

2.1 Air Model

2.1.1 IntroductionEPA has used the ISCST3/PERFUM air model to estimate fumigant concentrations in a variety ofsoil fumigation scenarios. However the applicability of the ISCST3 air model—and by extensionthe PERFUM model that is built on ISCST3—in scenarios where calms are important has beenquestioned,5 but not quantified. In what follows we will demonstrate that calm conditions andother factors leading to high atmospheric stability classes are critical for EPA to model in order tobe assured of realistic fumigant exposure estimates.

2.1.2 Recent Major PoisoningsIn this section we review four major fumigant poisonings that have occurred since 1999 inCalifornia (Table 2-1). The goal of the review is to identify common features, if any, in themeteorology leading up to the poisonings.

The poisonings were selected for availability of a combination of information, including theircapture in a detailed surveillance program,6 weather conditions, follow-up analyses, and size.Although these four poisonings are all from California, where this information is most available,there is no reason not to expect that they are representative of poisonings distributed in any statewhere fumigants are used.

Table 2-1: Selected Fumigant Poisonings, Number of Victims, and Crop (pre-plant) by Yearand Location

Year Location Fumigant Victims Crop1999 Earlimart7 Metam Sodium 170 Potato2002 Arvin8 Metam Sodium 273 Carrot2003 Thermal9 Metam Potassium 12 Unknown2003 Lamont10 Chloropicrin 166 Onion

We have identified the onset of poisoning (Table 2-2) in all four cases by either time of first callfor help or by victims’ accounts which contain times of onset of poisoning symptoms. In one ofthe cases, the data available to us just describes the time as “evening.” To assign a time to“evening”, we have used two hours after sunset. Our conclusions are not sensitive to this choice.

Table 2-2: Time of Onset of Poisoning by Location (as reported and in PST)

Location Onset of Poisoning as Reported In PSTEarlimart 1999-11-13 17:00:00 PST (PDT not in effect) 17:00Arvin 2002-07-08 18:30 PDT 17:30Thermal 2003-09-25 23:00 PDT 22:00Lamont 2003-10-04 "evening" 19:35


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We compared the poisoning onset times with sunset and wind data (Table 2-3). The sunset datacomes from readily available astronomical calculators.11 The wind data comes from the CaliforniaIrrigation Management Information System (CIMIS),12 a network of over 120 weather stationsdistributed throughout California. From this network, we selected the stations closest to thepoisoning incidents. The possibility of variations between the wind at the actual poisoning sitesand that at the selected CIMIS stations is a limitation of this analysis, but it does not impact theconclusions.

Table 2-3: Time of Sunset and Source of Weather Data by Location

Location Sunset CIMIS StationEarlimart 16:51 PST VisaliaArvin 19:13 PST Arvin/Edison (dataset I)Thermal 17:38 PST OasisLamont 17:35 PST Arvin/Edison (dataset II)

Sunset and weather data for California is typically reported in Pacific Standard Time (PST). Weconverted onset of poisoning times from the reports and eyewitness accounts that occurredbetween 2 am on the first Sunday in April and 2 am on the last Sunday in October from PacificDaylight Time (PDT) to PST by subtracting one hour.13

We plotted in Figures 2-1 through 2-4 the wind, time of sunset and time of onset of poisoning foreach incident.

CIMIS VISALIA STATION HOURLY WIND SPEED, 1999-11-13

0

2

4

6

8

10

12

0 4 8 12 16 20 24

Hour of Day (PST), Sunset (Solid Vertical), and Onset of Poisoning (Dashed Vertical)

Win

d S

pee

d (

MPH

)

Wind Speed (MPH) Sunset Onset of Poisoning

Figure 2-1: Earlimart, 1999, Wind, Sunset, and Onset of Poisoning

The Earlimart poisoning (Figure 2-1) is characterized by very low wind speeds throughout theday. (Wind speeds of a few miles per hour are comparable to those a pedestrian would feel whenwalking in perfectly calm air.) The Earlimart poisoning onset is at or shortly after sunset.


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CIMIS ARVIN/EDISON STATION HOURLY WIND SPEED, 2002-07-08

0

2

4

6

8

10

12

0 4 8 12 16 20 24


Win

d S

pee

d (

MPH

)Wind Speed (MPH) Sunset Onset of Poisoning

Figure 2-2: Arvin, 2002, Wind, Sunset, and Onset of Poisoning

The Arvin poisoning (Figure 2-2) is characterized by wind speeds dropping below 5 mph at theonset of poisoning. The Arvin onset of poisoning is shortly before sunset. Some accounts alsodescribed onset as “evening.”

CIMIS OASIS STATION HOURLY WIND SPEED, 2003-09-25

0

2

4

6

8

10

12

0 4 8 12 16 20 24


Win

d S

pee

d (

MPH

)

Wind Speed (MPH) Sunset Onset of Poisoning

Figure 2-3: Thermal, 2003, Wind, Sunset, and Onset of Poisoning

The Thermal poisoning (Figure 2-3) is characterized by wind speeds of approximately 3 mph atonset. The Thermal poisoning onset was approximately 4 hours after sunset.


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CIMIS ARVIN/EDISON STATION HOURLY WIND SPEED, 2003-10-04

0

2

4

6

8

10

12

0 4 8 12 16 20 24


Win

d S

pee

d (

MPH

)Wind Speed (MPH) Sunset Onset of Poisoning

Figure 2-4: Lamont, 2003, Wind, Sunset, and Onset of Poisoning

The Lamont poisoning (Figure 2-4) is characterized by wind speeds below 5 mph throughout theday. Onset of poisoning was described as “evening,” and this is plotted above as two hours aftersunset.

To summarize, a common and striking feature of the data is that all four cases occurred with windspeed less than 5 mph, and had onset shortly before, at, or after sunset. The significance of thiswill be discussed in a subsequent section.

2.1.3 Relative Frequency of Low Wind ConditionsIt might seem unlikely to associate pesticide drift incidents with low wind conditions because it iswind that is carrying the pesticides away from the application area. However, for the fumigantpoisonings examined above, low wind conditions are a common feature, and as we shall see in asubsequent section, an important feature. For this reason, we selected some weather data toquantitatively determine the percentage of hours that low wind conditions occur. We found thatlow wind speeds occur frequently, during at least 10% of the hours annually, and up to 30% ofthe hours depending on the cutoff defining low wind speeds14 and the weather stations used forthe estimates. The reader that already knows or anticipates this can skip to the next subsection.

We selected three stations in agricultural regions of California from a set of approximately 380nationally distributed Navy and National Weather Service (NWS) stations for which we have1999 data from a TD-3280 format dataset:15,16 In the TD-3280 dataset, stations are uniquelyidentified by Weather Bureau-Army-Navy (WBAN) ID. The purpose of Table 2-4 is simply touniquely identify the selected stations in some of the major weather station identificationschemes.

Table 2-4: WBAN ID, Call Letters & Place Name for Selected Stations in TD-3280 Dataset

WBAN ID17 Call Letters Place Name23155 KBFL Bakersfield, Meadows Field Airport23237 KSCK Stockton, Stockton Metropolitan Airport93193 KFAT Fresno, Fresno Air Terminal


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To gain insight into how often low wind conditions occurred over one full year at these stations,we binned the hourly wind speeds into 2 mph ranges (Table 2-5):

Table 2-5: Number of Hourly Wind Speed Measurements for a Given Speed Binned byWind Speed for Selected Stations in the 1999 TD-3280 Dataset

Station Bakersfield Fresno Stockton All TD-3280CALM AND NEAR-CALM 1405 1805 1126 4480313 to 4 mph 1052 1092 868 2552285 to 6 mph 2413 1957 2021 5986657 to 8 mph 1794 1481 1531 5612069 to 10 mph 1020 1045 1136 45354511 or more mph 1072 1372 2065 919734UNKNOWN 3 7 0 15818TOTAL 8759 8759 8747 3252227

A maximum of 24 * 365 = 8760 hourly readings in the year are possible. For the selected stationsa negligible number (less than 1/2%) are missing or unknown.

We next plotted (Figure 2-5) the same data from Table 2-5. We expressed the number of hourlywind speed measurements as a percentage of the total number of observations:

Bakersfield Hourly Wind Speed Distributions for 1999

% CALM AND NEAR-CALM16%

% 3 to 4 mph12%

% 5 to 6 mph28%

% 7 to 8 mph20%

% 9 to 10 mph12%

% 11 or more mph12% % CALM AND NEAR-CALM

% 3 to 4 mph

% 5 to 6 mph

% 7 to 8 mph

% 9 to 10 mph

% 11 or more mph

Figure 2-5: Wind Speed Distributions for Bakersfield KBFL Weather Station for 1999

In Figure 2-5 for Bakersfield, which is near three of the poisonings examined above, we see thatwind speeds of less than 5 mph occurred on 28% (16% calm and near-calm plus 12% 3 to 4 mph)of the hours in 1999.

In Figure 2-6 for Stockton, wind speeds of less than 5 mph occurred on 23% (13% calm and near-calm plus 10% 3 to 4 mph) of the hours in 1999.


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Stockton Hourly Wind Speed Distribution for 1999

% 3 to 4 mph10%

% 5 to 6 mph23%% 7 to 8 mph

18%

% 9 to 10 mph13%

% 11 or more mph23%


% CALM AND NEAR-CALM

% 3 to 4 mph

% 5 to 6 mph

% 7 to 8 mph

% 9 to 10 mph

% 11 or more mph

Figure 2-6 Wind Speed Distribution for Stockton KSCK Weather Station for 1999

In Figure 2-7 for Fresno, wind speeds of less than 5 mph occurred on 33% of the hours in 1999.

Fresno Hourly Wind Speed Distribution for 1999

% 3 to 4 mph12%

% 5 to 6 mph22%

% 7 to 8 mph17%

% 9 to 10 mph12%

% 11 or more mph16%

% CALM AND NEAR-CALM21% % CALM AND NEAR-CALM

% 3 to 4 mph

% 5 to 6 mph

% 7 to 8 mph

% 9 to 10 mph

% 11 or more mph

Figure 2-7 Wind Speed Distribution for Fresno KFAT Weather Station for 1999


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For all stations in the TD-3280 dataset combined (Figure 2-8), wind speeds below 5 mphoccurred on 22% of the hours in 1999.

All TD-3280 Hourly Wind Speed Distribution for 1999

% 3 to 4 mph8%

% 5 to 6 mph18%

% 7 to 8 mph17%

% 9 to 10 mph14%

% 11 or more mph29%


% CALM AND NEAR-CALM

% 3 to 4 mph

% 5 to 6 mph

% 7 to 8 mph

% 9 to 10 mph

% 11 or more mph

Figure 2-8 Wind Speed Distribution for All Weather Stations in TD-3280 Dataset for 1999

Note that the fraction of days on which wind speeds below 5 mph occurred is a priori boundedbelow by the fraction of hours on which they occurred. Therefore we can infer, for example, thatwind speeds of less than 5 mph occurred on more than 28% of the days at Bakersfield (16% calmand near-calm plus 12% 3 to 4 mph). This is a lower bound for the fraction of days of occurrenceof low wind speeds.

The conclusion of this analysis is that any model that performs poorly at low wind speeds isperforming poorly for a significant fraction of the days.

Here is a specific example to make the conclusion less abstract: If a model is used for Bakersfieldthat performed poorly in calm and near-calm conditions, then the model is performing poorly forat least 16% of the days. Any estimate of the number of hours for which a certain concentration isexceeded could be wrong for that fraction of the hours.

Even more specifically, use of the model and procedure EPA has used in the fumigant clusterassessment, which is to treat ISCST3 results for calm and near-calm hours as missing, guaranteesthat exposures for an area like Bakersfield have been underestimated on at least 16% of the days.

The data presented are for the entire year. The fraction of calm hours may be even larger if theanalysis is restricted to the months of peak fumigant application. Instead of weighting all days inthe 5-year simulation equally, EPA should use the weather data from just the months of peakfumigant application.

2.1.4 Evidence for High Atmospheric Stability ClassesIn this section, we will see that the conditions for the creation of high atmospheric stabilityclasses are present in the incidents we examined. To do this, we first have to introduce thestandard classification for atmospheric stability conditions.


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We have reproduced the Pasquill (or Pasquill-Gifford) stability classes in Table 2-6:18

Table 2-6: Pasquill Stability Classes

Surface Windspeed Daytime Incoming Solar Radiation Night-time Cloud Coverm/s mph Strong Moderate Slight > 50% < 50%<2 <5 A A-B B E F2-3 5-7 A-B B C E F3-5 7-11 B B-C C D E5-6 11-13 C C-D D D D>6 >13 C D D D D

Note: Class D applies to heavily overcast skies, at any wind speed, day or night

All of the poisonings in Table 2-1 occurred around or after sunset, with low wind speeds. We seefrom examining Table 2-6 that they generally occurred at the highest Pasquill stability classes (Eor F). These Pasquill stability classes are associated with the creation of ground level inversionlayers.•

It is striking that all the incidents examined occurred during Pasquill Stability classes E and F,since they were not selected for that. We conclude that on both theoretical grounds and on theexamination of major poisonings that it is critical to correctly model low wind speeds and highstability classes in the fumigants cluster analysis.

2.1.5 Additional Evidence for the Importance of High AtmosphericStability Classes

Working from the preceding section, we can now understand the significance of the followingeyewitness accounts from victims of the Earlimart poisoning:

1999-1252 - “It was around 5 o’clock when I saw some kind offog coming in but with a strong smell. Then less than a minute, acop came knocking on my door and told us to leave our homesbecause of a chemical going on [sic].”

• For completeness, we include the relationship of high Pasquill stability classes to ground-level inversionlayers, to which they are associated.

During the day, in direct sun, the earth heats up more quickly than the air. As the air near the earth iswarmed by the earth, convection occurs and this creates and deepens a layer of warm air above the earth.As the warming stops around and after sunset, a second effect takes over, which is that the earth cools morequickly than the air above it. The air near the earth is cooled by the earth. If there is little wind to causemixing of this cool air with the warmer air above it, an inversion layer occurs.

The cool layer is often visible to the eye because the water vapor in the layer condenses, and fog forms atground level. This condition is sufficiently common in the Central Valley, that it has a name, “Tule fog.”The cold air is dense and hence the fog settles into low areas. It therefore appears to be directly associatedwith streams and marshes which are also in low areas. It is actually caused not by the presence of thestreams and marshes, but by the cooling of air near the earth as just described. (However, surface water cancontribute to evaporative cooling.) The upper boundary of the fog is an indication of the height of theinversion layer, and an indication of the height to which mixing occurs. Any gases that are emitted from theearth will to a high degree be trapped in the same layer as is sometimes manifested to the eye as fog.


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1999-1234 - At around 5:00 p.m. on Saturday, November 13, a39-year-old, living on Dietz south of Avenue 48, reportednoticing an odor like burning rubber, and experienced eyeirritation, and irritation of the nose and throat. The materialcoming from the fields resembled a cloud or fog.

The arrival of the “cloud” or “fog” at the same time as the arrival of the poison gas we nowunderstand may not be a coincidence, nor does it necessarily have to relate to water vaporassociated with the “watering in” of the fumigant. Instead, the arrival of the fog may signal thearrival of an inversion layer.

A third account also has significance:

1999-1239: A resident of East Armstrong, 0.6 miles from thetreated field, noticed a strong odor in the late afternoon onSaturday, November 13, corresponding with a change in winddirection from south and east instead of the usual direction fromnorth and west.

A change in wind direction at a location generally means that wind at one location and wind atanother location are different. Where two bodies of air converge, a front condition can occur.Condensation can occur at the collision point of the air masses, and pollutants, particularly thosethat are heavier than air, can be concentrated there. It is possible that the victim’s account signalsa convergence.

So these accounts raise the possibility of either the entry into an inversion layer or the entry intoa front or convergence. Either situation can greatly concentrate pollutants.

2.1.6 Adequacy of PERFUM/ISCST3We have demonstrated in previous sections that it is not possible to have a compelling andquantitative understanding of the large poisonings we examined without accurate modeling of:

• Meteorology at low wind speeds• Insolation changes (e.g., sunset)• E and F Pasquill stability classes• Development of boundary layers, including concentration of pollutants within

boundary layers• Fronts, including concentration of pollutants at convergences

The PERFUM/ISCST3 is a simple Gaussian plume model that does not attempt to and cannotmodel all these conditions. In fact, its results under these conditions are sufficiently misleading atlow wind speeds that they are commonly thrown out of the overall results per EPA guidelines(see following sections). The borderline for discarding results that is commonly used is windspeeds of less than 2 mph (or 1 m/s), but this may in part be a proxy for high Pasquill stabilityclasses and the onset of the complex meteorology just described.

It is precisely this meteorology that describes the most dangerous conditions for the developmentof toxic fumigant concentrations, as demonstrated by examination of actual incidents. WhilePERFUM/ISCST3 has been used to model these conditions, and has obtained results consistent


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with reports of toxic exposures, the quantitative results could easily be an underestimate of theactual concentrations.

2.1.7 EPA Recommendations on Alternative ModelsGiven that the PERFUM/ISCST3 model is not adequate to model the relevant conditions, thequestion is what model to choose instead.

To guide specifically in this type of situation, EPA’s Air Quality Modeling Group (AQMG) hasmade available the Guideline on Air Quality Models, EPA 40 CFR Ch. I (7–1–03 Edition) Pt. 51,App. W,19 referred to in the remainder of this and the following subsections as The Guideline.

The following is the full text of paragraph 9.3.4.2 of The Guideline:

9.3.4.2 Recommendations

a. Hourly concentrations calculated with steady-state Gaussian plume modelsusing calms should not be considered valid; the wind and concentration estimates forthese hours should be disregarded and considered to be missing. Critical concentrationsfor 3- , 8-, and 24-hour averages should be calculated by dividing the sum of the hourlyconcentrations for the period by the number of valid or non-missing hours. If the totalnumber of valid hours is less than 18 for 24- hour averages, less than 6 for 8-houraverages or less than 3 for 3-hour averages, the total concentration should be divided by18 for the 24-hour average, 6 for the 8-hour average and 3 for the 3-hour average. Forannual averages, the sum of all valid hourly concentrations is divided by the number ofnon-calm hours during the year. For models listed in Appendix A, a post-processorcomputer program, CALMPRO has been prepared, is available on the SCRAM InternetWeb site (subsection 2.3), and should be used.

b. Stagnant conditions that include extended periods of calms often produce highconcentrations over wide areas for relatively long averaging periods. The standardsteady-state Gaussian plume models are often not applicable to such situations. Whenstagnation conditions are of concern, other modeling techniques should be considered ona case-by-case basis (see also subsection 8.2.8).

c. When used in steady-state Gaussian plume models, measured site specificwind speeds of less than l m/s but higher than the response threshold of the instrumentshould be input as l m/s; the corresponding wind direction should also be input. Windobservations below the response threshold of the instrument should be set to zero, withthe input file in ASCII format. In all cases involving steady-state Gaussian plume models,calm hours should be treated as missing, and concentrations should be calculated as inparagraph (a) of this subsection.

Note that this paragraph of The Guideline begins by underlining the inadequacy of Gaussianplume models under low wind conditions. In response to this, paragraph 9.3.4.2.c of TheGuideline describes a procedure for discarding calm and near-calm results fromPERFUM/ISCST3. However in the present case (fumigant gases originating at ground-level andbeing contained near the ground due to high atmospheric stability), discarding these results willresult in dangerously under-protective estimates of fumigant concentrations.

In this case, paragraph 9.3.4.2.b is applicable: “When stagnation conditions are of concern, othermodeling techniques should be considered on a case-by-case basis.” Until recently, the set ofconditions identified in the previous section surpassed the state-of-the-art in regulatory airmodeling.


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Fortunately, in the last several years—in fact during the very range of years that the poisoningswe have examined were occurring—the state-of-the-art in regulatory modeling has expanded toencompass these conditions. The American Meteorological Society has developed the AERMODmodel that goes beyond ISCST3 and contains new and improved algorithms for:20

1) dispersion in both the convective and stable boundary layers2) plume rise and buoyancy3) plume penetration into elevated inversions4) treatment of elevated, near-surface, and surface level sources5) computation of vertical profiles of wind, turbulence, and temperature6) the treatment of receptors on all types of terrain (from the surface up to and above the

plume height

The most important for of these for the present case is the first: dispersion in stable boundarylayers.

AERMOD, like ISCST3, is a steady state plume model and as such neither is designedfor completely calm conditions. But unlike ISCST3, AERMOD is designed to handlevery light winds. It does this, through the introduction of a meander algorithm. Themodel still requires some wind in order to define the mean wind direction and to estimatethe surface friction velocity. ISCST3 has no capability to account for light winds (lessthan 1 m/s), nor the expected effects of wind meandering during these conditions.Unfortunately AERMOD’s meander algorithm is not applicable to area sources. To takeadvantage of AERMOD’s meander algorithm for an area source, it is necessary to modelthe area source as a group of point sources.21,22

The process for the evaluation of alternative models is given in Section 3.2 of The Guideline. Inparagraph 3.2.1.a we read that:

Selection of the best techniques for each individual air quality analysis is alwaysencouraged, but the selection should be done in a consistent manner. A simple listing ofmodels in this guide cannot alone achieve that consistency nor can it necessarily providethe best model for all possible situations. EPA reports are available to assist indeveloping a consistent approach when justifying the use of other than the preferredmodeling techniques recommended in The Guideline.

An important point is that pre-selected lists of models are available, but do not necessarilyprovide the best model, and that EPA reports are available that provide assistance in modelselection.

In the case at hand, the evaluation of AERMOD, including evaluation of results relative toISCST3, has been performed by EPA. The evaluation demonstrates that in all 17 scenarios (10non-downwash scenarios and 7 downwash scenarios), there were either (a) similar results, (b)improvements, or (c) notable improvements over ISCST3.23,24,25

We conclude that AERMOD is an applicable and superior model for exposure modeling in thefumigants cluster assessment, and that EPA needs to perform its exposure modeling using such amodel in order to be confident of the protectiveness of its exposure estimates.


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2.1.8 Air Modeling ConclusionsIn summary, we have identified the most dangerous conditions for the development of highfumigant concentrations, both on theoretical grounds and by an examination of major poisonings.We have demonstrated that modeling of these conditions cannot be accomplished via ISCST3.Instead, the only model that has undergone extensive validation by the EPA and that can modelthese conditions is AERMOD. The procedure and model EPA is currently using is guaranteed tosystematically and severely underestimate exposures during a substantial fraction of the hours.

Following The Guideline, Section 9.3.4.2.b, EPA should recalculate the concentration estimatesusing an appropriate model. It is critical for this recalculation to incorporate realistic conditionsresulting in Pasquill stability classes E and F. Only then will we be confident of having realisticestimates of the high fumigant concentrations that have repeatedly poisoned agriculturalcommunities, and only then will we be in a position to understand whether and which riskmitigation strategies will end these poisonings.

2.2 Other Exposure Modeling ConsiderationsIn this section, we consider other issues in EPA’s preliminary risk assessment that could lead toinaccurate estimation of fumigant exposures.

2.2.1 Comparison of Exposure Modeling MethodologiesIn EPA’s technical briefing, the methodologies for exposure modeling are listed as:

• Field Volatility Monitoring Studies• EPA’s ISCST3 Model• PERFUM Model• Risk [Fully Probabilistic Risk Assessment]

and these are described as being in order of “increased predictive capability.”26

This is an incorrect characterization. In light of Section 2.1, we have already observed thatISCST3, and the PERFUM model on which it is built, fail during calm and near-calm conditions.

Any probabilistic risk assessment which builds upon the results of these models will incorporatethe same failures. Unless a better underlying model is used, the methodology that is most reliableis analysis of field studies and accounts of actual poisoning incidents.

A correct characterization is that a broader range of exposure scenarios can be considered usingmethodologies further down in the above list. Even with this more accurate characterization, onemust make the caveat that using the ISCST3 air model as the underlying model may cripple theaccuracy of the probabilistic risk assessment. The probabilistic risk assessment will producesystematically biased underestimates of exposures for whatever fraction of hours are calm ornear-calm.

2.2.2 Model Calibration, Flux EstimatesIn each of the four fumigant phase 3 preliminary risk assessments, there is a sub-section titled“ISCST3 Flux Method 3: Indirect Back-Calculation” (see Metam Sodium/Metam Potassium, p.39, Methyl Bromide, p. 23, Dazomet, p. 34, Telone, p. 29). In this sub-section one would expectto see a listing of all available studies considered (whether from the peer-reviewed literature or


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submitted by the registrants to EPA, and whether selected or not for use in the corresponding riskassessment), and a comparison of the flux profiles found in the studies. In fact, there are nofigures, graphs, or tables summarizing the flux profiles. Although there is one reference in thesesub-sections,27 it only analyzes a single field study (Oceano) for a single fumigant (methylbromide).

Given that flux estimates are absolutely critical for exposure estimates, this omission makes itimpossible to follow or comment on a critical part of EPA’s work. The presentation thereforefails to be transparent.

We request that EPA include the necessary details of its “indirect back-calculation” for eachfumigant. For each fumigant, an analysis should be presented for each application method. Andfor each application method, there should be an analysis of the various studies (whether or notthey were used or excluded). If different soil types, temperature conditions or other factorsyielded different results for the application method, those variations should also be analyzed andpresented. Limitations of each study should be discussed, and EPA’s rationale for reducing thevarious study results to a final flux rate should be explained.

We suggest presenting this information in a table to facilitate comparison of the various studyconditions and results. Such a table would include columns for:

• Date and Location• Monitoring Conducted by (e.g., CA DPR, registrant, et cetera• Application Rate (lbs active ingredient/acre)• Acres Treated• Soil Temperature• Distance of Monitoring Station to Field Border (feet)• Location of Stations Relative to Prevailing Wind Direction (Upwind, Downwind,

Variable)• Maximum Concentration at Distance (ng/m3)• Calculated Flux Range• Notes

An example of a similar table (Table 6-1) can be found after the discussion of MITC fieldstudies..

2.2.3 Corroboration of Calibrated Model with Actual IncidentsWhen an applicable air model (such as AERMOD) is chosen, and the model is calibrated usingthe back-calculation method, then the model should be applied to the known major poisoningssuch as those considered in Section 2.1.2, so that it can be satisfactorily demonstrated that themodel accounts for these poisonings. This builds confidence in using the model to determinewhether risk mitigation measures will eliminate such poisonings. Conversely, withoutdemonstrating that a model (including the parameters used to calibrate it) accounts for pastpoisonings, there should be some concern that risk mitigation measures based on the modelresults will not prevent future ones. We look forward to EPA’s reconciliation of their exposuremodel with poisoning incidents, including weather and application data.


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2.2.4 Use of Maximum vs. Whole Field MethodBoth maximum and whole field methods are discussed in EPA’s preliminary risk assessment.Since populations may live downwind of a field in the prevailing wind direction, it is important touse the maximum method for exposure assessment. The whole field method would average theconcentrations rather than protecting the most exposed population. This would not be adequatelyprotective.

2.2.5 Consideration of Exposure from Multiple Field Fumigations inthe Same Geographic Area and Time Period

A review of fumigant poisonings will reveal that neighboring fields are often treated insuccession. Given the off-gassing profile from a single fumigation, it is entirely possible thatfumigations occurring on one day will combine with fumigations from a nearby field on anotherday and result in concentrations that exceed those measured or calculated for a single field.

Restrictions on the number of treated acres considered in the risk mitigation stage will not bemeaningful unless time and separation restrictions between multiple applications are proposed.Such restrictions would have to be based on quantification of the concentration increases frommultiple fumigations.

2.2.6 Dismissal of Ambient ExposureEPA has dismissed concerns over ambient exposures, despite the fact that some of the ambientexposure estimates do in fact exceed their level of concern (in the case of both sub-chronic andchronic exposure). Furthermore, since the ambient exposure levels are near the level of concern,the conclusion that ambient exposure can be dismissed as irrelevant may be completely reversedby changes in the HEC estimates and the acceptable MOEs. Finally, usage trends have not beenanalyzed. For example, in 1997 in Kern County, California, the reported metam sodium usagewas 3,886,527 pounds. In 2003, it was 5,031,816 pounds. One expects this 30% increase tocorrespond to a similar increase in airborne MITC concentrations, and this, by itself may beenough to reverse the dismissal of ambient exposure as a concern.

EPA needs to do a more careful analysis, taking the cases that exceed their level of concernseriously in preparation for risk mitigation, computing the sensitivity to the HEC estimates whichthemselves are only preliminary, and the sensitivity to MOEs, and finally the sensitivity to usagetrends may invalidate older ambient concentration measurements and require mitigation in thefuture even in locations where it was not necessary in the past.

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3 Occupational Exposure Analysis

3.1 Number of WorkdaysThe number of days spent handling fumigants is underestimated. We support the extrapolation tomaximum label rates in these exposure assessments. However, in our opinion, the Agency’s useof geometric means rather than 95% percentile of PHED exposure data, and estimate of 20 daysof exposure for commercial applicators, 8 hours a day substantially underestimates exposure inCalifornia and elsewhere, where employees of commercial applicators work very long hours inpeak season, and use of fumigants is very high in some areas. The California Department ofPesticide Regulation assessment of metam sodium exposure indicates that commercial applicatorsmay handle metam sodium up to 200 days per year. Grower-applicators may handle the fumigantup to 23 days per year.28 In Florida, agricultural methyl bromide applicators work seven to tenhours a day over a two-month period.29 Similar exposure patterns can be assumed for methylbromide and 1,3 dichloropropene because use levels and patterns are similar.

3.2 Length of WorkdayThe length of workday is underestimated. Risk estimates assume maximum daily 8 hourexposures for handlers and for fieldworkers working near to fumigant treated fields. Theseassumptions will underestimate exposures to those handlers and field workers working 10 hour or12 hour days and leave them inadequately protected. The National Agricultural Worker Survey30

confirms that many workers work more than 50 hours a week, hence more than 10 hours per day.In California fieldworkers often work longer than 8 hours during the peak season and in fact donot receive overtime pay rates until they have worked 10 hours per day, compared with 8 hours inmost industries. Similarly, in its recent glove amendment to the Worker Protection Standard, EPApermitted the use of glove liners for 10 hours in a 24-hour period, in recognition that manypesticide applicators work for 10 hours per day. Additionally, fieldworkers and fumigant handlersmay also be subject to residential bystander post-application exposure and this should be takeninto account.

3.3 Dermal and Ocular ExposureDermal and ocular exposure estimates are needed. The Agency has significantly underestimatedfumigant handler exposure by declining to estimate eye and dermal exposure of handlers tomethyl bromide and to MITC released during handling of metam sodium. The Agency’s 2002review of methyl bromide incident reports shows that over half (83 of 154) methyl bromideapplicator illnesses reported in California in 1982-1999 affected the skin or eyes. These illnessesincluded symptoms of blisters, contact dermatitis, eye irritation, burning eyes, skin burns anditchy rashes.31 CDPR has completed dermal exposure estimates for metam sodium handlers usingsurrogate sodium tetraborate exposure data that may serve as a model for estimating methylbromide handler dermal exposure.32


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Goggles and face shields typically used as protective gear in pesticide handling are designed forsplash protection, not vapor protection. These risk assessments fail to discuss how goggles andface shields can contribute to protection of the eye from fumigants.

3.4 Respiratory Protection FactorsRespiratory protection factors are overestimated. These risk assessments show that air-purifyingrespirators provide inadequate protection for a majority of fumigant handler tasks and in fact,margins of exposure are underestimated because of the Agency’s assumption that half-maskrespirators can be relied upon to provide a 10 -fold protection factor under agricultural pesticideuse conditions. The pesticide applicator respiratory protection regulations incorporated in theWorker Protection Standard (WPS) and California pesticide use regulations33 are much lessprotective than OSHA respirator regulations34, particularly in the area of fit-testing of respiratorsto prevent leakage. The current DPR regulation merely requires "written operating procedures forselecting, fitting, cleaning and sanitizing, inspecting and maintaining respiratory equipment." Thefederal WPS merely requires that respirators be cleaned and maintained without any fit testingrequirements. A correlation was found between depressed cholinesterase levels and use of half-mask respirators in a recent study of cholinesterase monitoring results of agricultural pesticideapplicators in the state of Washington.35

By contrast, the OSHA regulations proscribe specific protocols for qualitative and quantitativefit-testing of respirators. The OSHA regulations were tightened over five years ago, but the USEPA has yet to initiate any upgrade of pesticide handler respirator fit-testing requirements.

3.5 Respirator Cartridges and Canisters

3.5.1 Respirator Cartridges and Canisters for Methyl BromideThe methyl bromide risk assessment inappropriately recommends organic vapor respiratorcartridges and canisters for mitigation of methyl bromide handler inhalation exposure. Standardorganic vapor cartridges are not allowed for use in methyl bromide handling in California becauseof methyl bromide’s poor warning properties and evidence that methyl bromide does not adsorbwell to charcoal, especially under very humid or very dry conditions.36 It is our furtherunderstanding that manufacturers of standard organic vapor cartridges do not recommend themfor use in methyl bromide atmospheres.

We are aware that at least one manufacturer (3M) produces a special organic vapor cartridgewhich it recommends for use in atmospheres containing less than 5 ppm methyl bromide. This60928 cartridge uses a triethylenediamine (TEDA) impregnated charcoal for its absorption bed.However, we are also concerned that fumigation workers may not be adequately or reliablyprotected by use of respirators equipped with such cartridges for the following reasons: (1) NoUS governmental agency has conducted independent review of the manufacturer's testing of thiscartridge in a methyl bromide atmosphere. To the best of our knowledge, US EPA and DPR havenot even obtained results of individual tests, number of replicates, or calibration of equipmentused in manufacturer’s tests. We feel that independent review is particularly important forcharcoal-based cartridges used to protect against methyl bromide because, as mentioned above,research which DPR has conducted shows that methyl bromide, unlike many other volatileorganic compounds does not adsorb well to charcoal based sampling tubes. In addition, aspreviously mentioned, methyl bromide has very poor warning properties because it has almost noodor even at very high exposure levels.


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DPR has informed us previously that the detection limit for these tests was 0.2 ppm or 200 ppb. 37

We fail to understand how US EPA or DPR can rely on these data to conclude that workers areprotected to air concentrations more than ten-fold lower than the detection limit used by themanufacturer.

3.5.2 No Explanation for Protection Factors Assigned to EngineeringControls

These risk assessments do not include any explanation of how protection factors were assigned toengineering controls, which are described in table footnotes as closed mixing and loading systemsand enclosed cabs. Enclosed cabs should not be assumed to provide any protection frominhalation exposure of fumigant vapors unless they are equipped with special charcoal filters andthe filters are regularly changed and checked for leakage around the seals. A recent evaluation oftractor cab filtration systems identified the need to evaluate these filtration systems for leaksources.38

3.5.3 No Consideration of Heat Stress PreventionThese risk assessments fail to acknowledge that workers wearing respirators, synthetic coverallsand other protective gear are at elevated risk of heat illness, particularly when working in thedirect sun. It is not possible to move this work to the night, because stagnant night-time airconditions cause high-concentrations of off-site fumigant movement. Fumigant applicationshould be restricted to day-time conditions when the risk of heat stress will not be excessive forhandlers wearing protective equipment. This is consistent with limiting fumigant applications totimes when soil and air temperature are cooler in order to reduce off-site movement of fumigants.

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4 Methyl Bromide Toxicology

4.1 Selection of Critical Toxicity Study Endpoints for RiskAssessment

4.1.1 Acute ToxicityThe selection of the toxicity endpoints for acute methyl bromide toxicity from inhalation ordietary exposure is adequately supported by the data and the studies available to US EPA.

4.1.2 Subchronic (Intermediate) ToxicityWe do not agree with the choice of study and dose selection for the assessment of short-term andintermediate methyl bromide exposure and human health risks. We conclude that an estimatedNOAEL of 0.5 ppm (0.14 mg/kg-day) should be used for assessing short-term and intermediaterisk of methyl bromide exposure. This NOAEL is estimated by dividing the LOAEL of 5 ppm fordecreased responsiveness in dogs observed after 34 exposure days (Newton 199439) by a factor often. The use of a ten-fold uncertainty factor to extrapolate from a LOAEL to a NOAEL usingthese data is consistent with the ten-fold uncertainty factor applied by US EPA whenextrapolating from a LOAEL to a NOAEL, where a true NOEL (no observable effect level) is notevident from available data.40

For the past three years, there has been much scientific discussion in California regarding the twoavailable non-The Guideline methyl bromide toxicity inhalation studies conducted in dogs(Newton 1994 and Schaefer 200241). Two departments in the California Environmental ProtectionAgency (Cal/EPA), CDPR and the Office of Environmental Health Hazard Assessment(OEHHA), have documented their scientific interpretations of these studies. We have reviewedboth the Schaefer (2002) and the Newton (1994) studies, as well as the analysis prepared by USEPA’s Hazard Identification Assessment Review Committee,42 the relevant documentationobtained from both CDPR43, 44 and OEHHA,45 the National Research Council Review46 ofCDPR’s 1999 draft risk assessment, and the guidelines for conducting toxicity studies developedby US EPA.47,48 We believe that the analysis and comparison of the two methyl bromidesubchronic dog studies conducted by OEHHA49 is the best source of information regarding theuse of these studies in risk assessment to protect human health. Based on our review we havearrived at the following conclusions:

a) The dog is clearly the most sensitive species tested for methyl bromide toxicity.

b) Although neither the Newton (1994) nor the Schaefer (2002) study meets the USEPA guidelines for conducting a subchronic (90-day) inhalation study or for theneurotoxicity screening battery, the data are acceptable for risk assessment purposes.

c) There have been no reported problems in the study design or conduct to suggest thatthe toxicity finding reported by a neurotoxicologist of reduced responsiveness at5.3 ppm in Newton (1994) was not reliable or valid.


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d) There is no scientific basis for giving more or equal weight to the finding ofdecreased proprioceptive placing at 10 ppm in Schaefer (2002) compared to theneurotoxic effect noted at 5.3 ppm in the Newton (1994) study. Using 10 ppm as theLOAEL is not protective of public health.

e) The results of the Schaefer (2002) study are consistent with the Newton (1994)results, albeit the toxicity occurs at higher doses in the former study. Because theaccepted risk assessment methodology is to select the lowest dose with acorresponding toxicological effect, the Schaefer (2002) results support the selectionof 5.3 ppm from the Newton (1994) study as a LOAEL.

f) OEHHA and US EPA (in its 2003 Hazard Identification Assessment ReviewCommittee report) reach the same conclusions regarding the validity of the methodsand results, identification of the key toxicity endpoint, dose levels, and that the use ofthe Newton (1994) data is appropriate for risk assessment of subchronic(intermediate) inhalation exposures to methyl bromide.

g) For the purposes of risk assessment and mitigation, the results of the Newton (1994)study provide sufficient evidence for the most sensitive toxic effect of methylbromide (i.e., decreased responsiveness in dogs) to be used as the critical and mosthealth-protective end point for short-term and intermediate-term methyl bromideexposures in residents and workers.

As mentioned above, in 2003, after reviewing and comparing both dog studies, US EPA made thedetermination that the Newton (1994) study was the most appropriate from which to derive thetoxicity endpoint (LOAEL of 5.3 ppm) for intermediate (as well as chronic) methyl bromideexposures. Inexplicably, in the 2005 risk assessment, US EPA changed its determination toinstead select the lowest dose tested in the Schaefer (2002) study of 5 ppm as a NOAEL forintermediate exposures. This is an important decision in that the higher NOAEL used in USEPA’s methyl bromide risk assessment results in estimated risks that are about ten-fold lowerthan the estimated risks using the 2003 NOAEL determination.

US EPA states in its 2005 risk assessment that “endpoint selection will be based on the endpointsoccurring at the lowest HECs (which may or may not be the lowest animal NOAEL) derivedusing the RfC methodology.” Given that the toxicity thresholds for the neurotoxicity endpointsare identified from studies with essentially the same study design, then it is reasonable toconclude that the HECs derived from the data taken from these two studies would be comparable.It is clear that the Newton (1994) results provide the lowest HEC for short-term and intermediateinhalation risk assessment. Therefore we do not understand why US EPA adopted a less healthprotective human equivalent concentration.

The fact that US EPA offered no explanation for this critical and significant change in itstoxicology assessment is, at the very least, a symptom of the overall lack of clarity and detailprovided in the document. A more damaging interpretation is that US EPA has settled on acompromise based on political pressure to protect business interests. This is perhaps the mostimportant flaw in US EPA’s risk assessment for methyl bromide and the use of the proposedNOAEL of 5 ppm for short-term and intermediate exposures is not adequately protective ofhuman health. To reiterate, the scientific evidence fully supports that an estimated NOAEL of 0.5


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ppm (0.14 mg/kg-day), derived from the Newton (1994) data, should be used for assessing short-term and intermediate risk of methyl bromide exposure.

4.1.3 Chronic ToxicityThe selection of the chronic inhalation toxicity endpoint also presents a problem. Although it isunderstandable that US EPA desires to use the chronic rat study because the study design meetsUS EPA guidelines for conducting chronic and carcinogenicity inhalation studies in rodents, thescientific evidence supports the determination that dogs are the most sensitive test species tomethyl bromide exposure. In 2003, US EPA50 had recommended using the Newton (1994) dogstudy for chronic inhalation exposure risk assessment. This would be an acceptable approach. IfUS EPA insists on using the basal cell hyperplasia toxicity endpoint in rats51 (LOAEL = 3 ppm)as the endpoint for chronic inhalation toxicity, then an additional uncertainty should be included(see discussion below). This use of the rat endpoint is consistent with CDPR,52 which used anestimated NOAEL of 0.3 ppm in its 2002 risk assessment for inhalation exposures to methylbromide.

There is also a discrepancy between CDPR and US EPA in the selection of the study, criticalendpoint, and dose for chronic dietary risk assessment. In its 2002 risk characterization documentfor dietary methyl bromide exposure,53 CDPR selected the 1996 chronic oral dog study conductedby Newton, and a NOAEL of 1.5 ppm for decreased hemoglobin and/or hematocrit levels in maledogs. US EPA’s decision to use a NOAEL of 50 ppm from a rat study is: a) inconsistent with thewidely accepted methodology to select a toxicity endpoint from the more sensitive species whenthere are adequate toxicity data available in more than one species, b) does not result in the lowesthuman equivalent concentration, and c) is inconsistent with CDPR, something that US EPAstated it was trying to avoid. We recommend that the more health-protective toxicity endpoint anddose level of concern (1.5 ppm) from the dog study be used in the dietary exposure riskassessment.

4.2 Toxicology Data GapsWe find it particularly troubling that after almost 20 years of intensive evaluation of the healtheffects and risks of methyl bromide exposures, there is still a data gap for a developmentalneurotoxicity study, a key study for evaluating effects on what is probably the most vulnerablesubpopulation for methyl bromide toxicity. We understand that the Registrant has finally initiatedthe study, however it may take months to years for US EPA to evaluate the findings, validate theresults, and decide how the data should be used. When the study results are available, we urge USEPA to release them to the public to allow for further discussion and analysis of methyl bromidetoxicity and risk. Furthermore, we request that any changes made to the risk assessment formethyl bromide based on the results of this study be disseminated for public review andcomment.

4.3 Dermal Exposure Risk AssessmentAccording to both US EPA and CDPR, methyl bromide is highly toxic by both the dermal andocular routes of exposure (Toxicity Category I). However, based on a flawed assumption that oneor both of these exposure routes would not be expected for humans, a risk assessment fordermal/ocular exposure was not included in the assessment. There are enough occurrences ofspills and whole body exposures described in the methyl bromide toxicity incident reports towarrant a risk determination via dermal/ocular exposure. In fact, on August 29, 2005, a ModestoBee newspaper article described a worker who was sprayed in the face and eyes with methyl


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bromide, the result of faulty equipment. We urge US EPA to include this analysis in the riskassessment, especially for workers. Furthermore, an aggregate exposure/risk assessment mustinclude dermal exposures along with all other routes of exposure.

4.4 Uncertainty Factors

4.4.1 GeneralIn general, the discussion and justification for the use of uncertainty factors in the methyl bromiderisk assessment is difficult to follow and the rationale for selecting uncertainty factors so unclearas to appear as if US EPA’s decisions were subjective and arbitrary. We recommend that US EPAadopt the more widely used and recognized methodology in risk assessment for deriving levels ofconcern for humans from toxicity data. That is, dividing NOAELs by factors of ten (or factors ofthree only when adequate data and scientific support are available and a complete discussionprovided) to correct for interspecies and intraspecies variation, converting LOAELs to NOAELs,and for addressing adequacy or uncertainty in the database.

4.4.2 Further Protection of Infants and ChildrenIn 2001, US EPA concluded that an additional uncertainty factor of ten should be “retained” formethyl bromide54 as required by the Food Quality Protection Act of 1996 to address weight-of-evidence considerations and the differential toxicity between infants and children and adults. In2003, US EPA reversed its decision and concluded that no additional uncertainty factor waswarranted because the database is complete. At that time, the only new data to be submitted to USEPA was the Schaefer (2002) dog study previously addressed in these comments. In other words,there were no additional or new data available to US EPA specifically addressing developmentalneurotoxicity or the differential effects of methyl bromide on the developing fetus, infants, andchildren. This apparently arbitrary decision was not discussed in the 2005 risk assessment.Nevertheless, if this change remains in the risk assessment, the result is that the developing fetus,infants, and children will not be afforded additional protection compared to adults when exposedto regulatory levels considered acceptable to US EPA.

There are several scientific and public health policy arguments to justify additional protection forchildren and infants, as presented below. From a regulatory perspective, there is a data gap for adevelopmental neurotoxicity data. This is a key missing study because the available data fromgeneric developmental toxicity studies do not specifically address the most sensitive endpoint ofconcern for methyl bromide, which is neurotoxicity. The observed developmental toxicity,neurotoxicity, and genotoxicity of methyl bromide in experimental studies are other factors, as isthe observed difference in sensitivity for the developing fetus and newborn with methyl bromideexposure, when compared to adults. Furthermore, there is a wide variation in responses to methylbromide toxicity observed in exposed adults. Therefore, the conventional ten-fold uncertaintyfactor applied for human variability might only account for adult variation, and not fordifferences between adults and infants and children. Some, but not all, of the observed differencesin sensitivity among fetuses, newborn infants, developing young, and adults are overlapping.Nevertheless, we conclude that the scientific evidence supports that an additional uncertaintyfactor of ten be used in calculating the target concentrations in air, water, and the diet for methylbromide that are fully protective of infants and children. Therefore, we recommend that US EPAapply the default 1,000-fold uncertainty factor to the rat study LOAEL in order to define thechronic, non-carcinogenicity level of concern for the risk assessment.


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Data GapA reference dose or reference concentration to establish guidelines for human exposure for non-carcinogenic effects is usually determined by dividing the observed NOAEL from anexperimental animal study by an uncertainty factor of 100. The conventional uncertainty factor of100 includes a factor of ten for inter- and a factor of ten for intra-species differences. In its 1993report,55 the National Academy of Sciences (NAS) stated, “to provide added protection duringearly development, a third uncertainty factor of 10 is applied to the NOEL to develop the RfD.This third 10-fold factor has been applied by EPA and FDA whenever toxicity studies andmetabolic/disposition studies have shown fetal developmental effects.” NAS further stated that“Because there exist specific periods of vulnerability during postnatal development, thecommittee recommends that an uncertainty factor up to the 10-fold factor traditionally used byEPA and FDA for fetal developmental toxicity should also be considered when there is evidenceof postnatal developmental toxicity and when data from toxicity testing relative to children areincomplete.” This developmental neurotoxicity data gap alone might justify the need for anadditional uncertainty factor to protect the developing fetus, infants, children, and other moresusceptible subpopulations from exposure to methyl bromide.

NeurotoxicityNeurotoxicity is the predominant toxic effect of methyl bromide observed in most acute,subchronic, and chronic studies conducted in animals. An important aspect of methyl bromide-induced neurotoxicity is the persistence of effects after the termination of exposure, indicatingpotential irreversibility. The persistence of effects may be due to cumulative toxicity afterrepeated exposure to low doses. Examples in support of this mechanism of action are provided inthe 2002 addendum to the risk characterization document for inhalation exposure to methylbromide prepared by CDPR. Compared to exposures to toxic substances later in life, exposuresincurred early in life can lead to a greater risk of chronic adverse health effects such as cancer,irreversible neurodevelopmental impairment, and immune system dysfunction. According toNAS (1993), “Because so many bodily functions are at various stages of development throughoutinfancy and early childhood, toxic effects of chemical agents during these age periods not onlyproduce the same sorts of direct injuries to established organ tissues and function seen in adults,but also have the potential to affect the later development of anatomic, physiologic and metabolicprocesses. The nervous, immune and reproductive systems continue to develop after birth;therefore any toxic effects incurred during postnatal developmental stages of these systems mayhave lasting consequences throughout adult life.”

The toxic effects of methyl bromide on the developing central nervous system (CNS) are ofparticular concern. A human infant or young animal may respond quite differently than the adultof its species to toxic substances. The National Academy of Sciences (NAS) states in its 1993report that “Because of the evolving development of various organs and tissues, the effect ofexposure to toxic substances will vary in a complex way with the age at exposure. Substances thatare toxic to adults may have minimal effects at one stage of development, but at another stagethese same substances may produce permanent damage to the organism or may be lethal. Sucheffects are particularly prominent for the central nervous system.” Furthermore, the NAS reportstates that “Because human brain development continues for years after birth, it can behypothesized that postnatal exposure to xenobiotic compounds would alter the structure orfunction of the human nervous system.”

The central nervous system in developing individuals is potentially vulnerable for a protractedperiod because it requires longer than most other organ system for cellular differentiation,


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growth, and function organization. Furthermore, the developing nervous system is especiallyvulnerable because brain weight in infants and children is proportionately greater than in adults,and the cerebral blood flow is greater per mass unit of brain weight in children. Therefore, “anyincrease in accessibility to cytotoxic agents because of delayed maturation of the blood-brainbarrier could have serious consequences” NAS (1993). In its conclusion, NAS stated, “Despitethe difficulties in measuring effects, exposure to xenobiotic compounds has been found to alterCNS development at the anatomic and functional level. The alteration in development can beirreversible thus resulting in permanent loss of function. These damaging effects of xenobioticcompounds on CNS of the developing organism can occur at exposure levels that are safe for theadults.”

GenotoxicityMethyl bromide has been shown to be genotoxic in multiple in vitro and in vivo genotoxicityassays. Methyl bromide is also a direct-acting mutagen and has been shown to alkylate DNA oftissues from different organs in vivo. There is some evidence of methyl bromide-inducedgenotoxicity in humans.56 The ability of methyl bromide to interact with genetic material mayresult in greater impact on the young compared to adults. Children may be more susceptible thanadults to carcinogenesis or mutagenesis because, as developing organisms, their rate of growthand by corollary, cell proliferation, is much greater.

Differential SensitivityThe overall evidence from the toxicological profile of methyl bromide suggests that thedeveloping fetus, infants, and children are more sensitive than adults to the primary toxic effectsof methyl bromide on the central nervous system. One case report of an accidental exposure of aninfant and the infant’s parents to methyl bromide demonstrated the greater sensitivity of thedeveloping young to methyl bromide toxicity.57 In addition to pharmacokinetic sensitivities, thedeveloping nervous system is exquisitely sensitive to perturbations compared with the adultsystem. Given the data demonstrating that methyl bromide is a neurotoxicant, and the absence ofa robust developmental neurotoxicity test for methyl bromide, we believe that EPA is bound toapply the full 10X FQPA according to the law.

Methyl Bromide MetabolismIt is thought that methyl bromide conjugation with glutathione via glutathione transferase (GST)plays an important role in the metabolism/detoxification of methyl bromide, including methylbromide induced neurotoxicity. There is a broad genetically determined polymorphism inglutathione transferase activity among humans referred to as “fast and slow conjugators.”58 Thereare also ethnic differences in the prevalence of the genotype.59 The polymorphism of glutathionetransferase activity may result in different dose responses among individuals in a population withvarying toxic responses to methyl bromide exposure. Therefore, these differences in metabolism(conjugation) may be a factor in identifying susceptible subpopulations that would require moreconsideration in the risk assessment. Although the amount of data on the subject matter is limited,we recommend that such a discussion be included in the risk assessment. In humans, GSTdevelops before the eleventh week of gestation and does not change rapidly. Depending upon thegenetic combination of various alleles, a more then 100-fold difference in isozyme activity hasbeen reported among adults60 and a five-fold difference between adults and fetuses’ GST levels.61

Additional uncertainty should be incorporated in the assessment of the risk for the developingfetus, infants, and children to account for the uncertainty and variability in the data available ofmethyl bromide metabolism.


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ConclusionConsidering this scientific evidence as a whole, an additional ten-fold additional uncertaintyfactor to protect infants and children is warranted due to the uncertainties associated with thedifferential toxicity findings between developing and adult animals, case reports of humanexposures, and the genetic polymorphisms that exist for the metabolism of methyl bromide.

4.4.3 Chronic Toxicity Uncertainty FactorThe preliminary risk assessment for chronic inhalation risks defines the level of concern as theLOAEL from a chronic toxicity/carcinogenicity in rats divided by an uncertainty factor of 100.The universal risk assessment default is to apply a 1,000-fold uncertainty factor when no NOAELis identified from a toxicity study in animals. However, in its risk assessment US EPA assumes:a) their RfC methodology already accounts for a three-fold interspecies difference, and b) thetoxicity endpoint, basal cell hyperplasia, is not severe enough effect to warrant the full defaultuncertainty factor value of ten-fold for the extrapolation of a NOAEL from a LOAEL.

This logic is flawed on three grounds. First, as mentioned above, rats are less sensitive to methylbromide toxicity than dogs. This could mean that the interspecies differences between humansand experimental animals are underestimated. One solution is to use the intermediate termtoxicity study results of Newton (1994) for chronic toxicity as proposed by US EPA in 2003.However, the studies in dogs were not designed to be chronic toxicity/carcinogenicity studies. Amore practical solution is to use a larger uncertainty factor in deriving the levels of concern.

4.4.4 CarcinogenicityMethyl bromide is a direct-acting mutagen, especially in in vitro systems. It was found positive inSalmonella typhimurium strains TA 100 and TA 1535, Escherichia coli strains Sd-4 and WP2hcr,and in Saccharomyces cerevisiae. It also produced a dose-dependent induction of sex-linkedrecessive lethality in Drosophila melanogaster. In in vivo assays, methyl bromide was found tocause dominant lethal mutations, an increase of micronuclei, and a dose-related increase in thefrequency of sister chromatid exchanges in bone marrow. DNA adducts were detected in liver,lung, stomach, and forestomach of rats exposed to high concentration of methyl bromide byinhalation. Although there is no clear evidence of oncogenicity in the currently availablechronic/carcinogenicity studies in animals, CDPR in its Summary of Toxicological Data forMethyl Bromide, does describe some data that are suggestive of carcinogenic potential. This is asignificant biological contradiction. The lack of correlation between the strong mutagenic activityand the largely negative results in cancer bioassays for methyl bromide is significant enough towarrant discussion in the risk assessment as well as some added degree of uncertainty in theresults.

Finally, there is recent evidence that methyl bromide increases the incidence of prostate cancer inmale agricultural workers (applicators).62 The Agency’s classification of methyl bromide as “notlikely to be carcinogenic in humans” fails to encompass a growing body of epidemiology. Arecent large prospective cohort study conducted by the National Cancer Institute of 55,332 malepesticide handlers in two states (Iowa and North Carolina) found use of methyl bromidesignificantly associated with heightened risk of prostate cancer. The association had an exposure-related trend with odds ratios of 2.73 (95% CI 1.18, 6.33) and 3.47 (95% CI: 1.37, 8.76) in thetwo highest exposure categories.63 Moreover, a study of California farmworkers (ecologicalepidemiology study design) found a suggestion of elevated risk of prostate cancer amongfarmworkers judged to have high exposures to methyl bromide as assessed from pesticide use


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records for crops, counties and time periods of work. The Odds Ratio was 1.16 (95% CI: 0.77,1.75).64 Virtually no discussion of this study is included in the 2005 risk assessment or any of thepost 2003 memoranda and documents produced by US EPA staff. This is an important oversightthat must be corrected.

The new human evidence linking methyl bromide exposures with increased risk of cancercoupled with the strong evidence of genotoxic and mutagenic potential of methyl bromidesupports our determination that EPA needs to conduct a thorough and transparent scientific re-assessment of the cancer risk associated with methyl bromide. This assessment should undergopublic review by a Scientific Advisory Panel that includes authors of the main epidemiology andecological studies of methyl bromide cancer risks. Presuming that a risk of cancer is found to beassociated with methyl bromide, EPA should conduct a quantitative risk estimate (Q*) presuminglinearity at low exposures. The EPA 2005 Cancer Guidelines Supplemental65 are clear that wheninfants or children may be exposed, the default assumption is to assume no safe level of exposure,and use a linear low dose extrapolation for mutagens. The EPA assessment of methyl bromidecancer risks will have no credibility or scientific defense if EPA fails to conduct a thorough andtransparent review of the cancer risks for methyl bromide consistent with the 2005 CancerGuidelines.

4.5 Cumulative Risk Assessment: Chloropicrin Plus MethylBromide

Chloropicrin is combined with methyl bromide as a warning agent and also as an activeingredient. Chloropicrin is used with methyl bromide in various products at ratios varying fromapproximately 1:400 to 1:1. In California, 4.93 million pounds of chloropicrin were reported usedin 1997, compared to 7.38 million pounds of methyl bromide (Pesticide Use Report, CDPR,2003). This is particularly relevant in applications to strawberries, for which reported methylbromide use in 2003 was 3.67 million pounds, and reported chloropicrin use was 3.28 millionpounds (presumably applied together).

US EPA includes a brief discussion of the public health data regarding chloropicrin/methylbromide formulations in its risk assessment. However, there is not enough information toadequately convey the impact of combining these two active ingredients on human health. Wehave provided general comments regarding US EPA’s methods to evaluate cumulative risks ofthe soil fumigants (see Section 1.5). It is essential that US EPA quantify the health risks of theexposure to the combination of methyl bromide and chloropicrin, including a completetoxicological evaluation of combined toxicity, exposure, and interaction between chloropicrin andmethyl bromide to address the risk of using these formulations.

When US EPA completes its assessment for chloropicrin as an active ingredient, we believe thatthe findings will demonstrate that chloropicrin is much more acutely toxic than methyl bromide(up to about 50 times more potent as an irritant). Therefore, we believe that the effects ofchloropicrin, and not methyl bromide will dominate the acute toxicity hazard from the use ofchloropicrin/methyl bromide mixtures. In addition, because the volatility and evaporation rate ofchloropicrin is lower than that of methyl bromide, it is likely that chloropicrin persists longer inthe environment. Therefore, measured levels of methyl bromide in ambient air would notaccurately predict chloropicrin levels based on the initial mixture ratio. It appears that the longer-


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duration inhalation exposures from use of the combined products could be essentiallychloropicrin exposure.

We have already alluded to the polymorphism of glutathione-S-transferase (GST) enzymes inhumans and the role of GST in mediating methyl bromide toxicity. Because GST also activateschloropicrin66 there is clearly a need for US EPA to research the association between themechanism of action and the cumulative toxicity of these two agents.

In looking toward the future for assuring worker and public health and safety related tofumigants, we remain concerned about the absence of regulatory controls specific to chloropicrin,an agent with high acute toxicity, and chloropicrin used in combination with methyl bromide andother fumigants. Some registered methyl bromide products currently contain up to 50%chloropicrin, thereby increasing our concern regarding this agent. Even if methyl bromide usecontinues, or if its use declines or is phased out altogether, it is likely that some growers willchoose to use other fumigant that also utilize chloropicrin as an active ingredient and warningagent. Since products containing chloropicrin are being re-evaluated for registration purposes atthis time, it seems appropriate and timely that US EPA initiate rule making for chloropicrin, as itis used in combination with other soil fumigants, in particular methyl bromide and Telone. Webelieve that when assessed together, the combination of the toxicity levels of concern and theexposure risks for residents and workers will require even more stringent mitigation and controlmeasures than the use of either of these chemicals alone. It is quite possible that the data willdemonstrate that there is no acceptable means to handle mixtures of methyl bromide andchloropicrin.

4.6 Aggregate Risk AssessmentFor methyl bromide, there are four distinct sources of exposure in the environment and workplace(air, water, diet, and direct contact) and three important exposure routes (inhalation, ingestion,and dermal contact). An appropriate aggregate risk assessment for a single chemical considers allroutes of exposure together to characterize short-term (acute), intermediate (subchronic) andlong-term (chronic) risks. Although the toxicity endpoint often differs in animal studiesdepending on the route and duration of exposure, for methyl bromide there are commonendpoints for which aggregate risks can be estimated. At a minimum, these toxicity endpointsinclude neurotoxicity, weight loss, and developmental effects.

The sections referring to aggregate risk assessment are so poorly written that is not clear whatapproach US EPA has taken in deriving aggregate risks for methyl bromide. The document doesnot present a useful characterization of risks from exposure through multiple exposure routes.Therefore, the risk assessment is incomplete in this regard. Most likely, inhalation risks woulddominate an aggregate risk assessment, especially for subchronic and chronic toxicity. However,dermal exposure is especially critical for acute exposures in workers, but was completely ignoredby US EPA. We recommend the authors revise the risk assessment document to include a fullquantitative analysis of all three exposure routes and all four exposure sources and provide a tableshowing aggregate risks for acute, subchronic and chronic exposure to methyl bromide.

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5 1,3-Dichloropropene Toxicology

5.1 Use of Human Equivalent Concentration MethodologyWe have serious concerns about the use of the Human Equivalent Concentration (HEC)methodology to estimate human No Observed Adverse Effect Level (NOAEL) values for 1,3-D.One major concern is that the documentation provided does not provide any scientificjustification for the choice of an uncertainty factor of three instead of ten. No calculations areshown for the conversions between NOAELs and HECs throughout the document, which meansthat it is impossible to evaluate the specific values used for minute volume, surface area, andRGDRs used for interspecies extrapolation. Nor is any information provided on the specificdosimetric adjustments EPA made based on the physicochemical properties of 1,3-D, and how,precisely, the Agency is taking into consideration the pharmacokinetic differences betweenanimals and humans. This risk assessment is not complete without this information. US EPAmust provide the scientific information on which its decisions are based. Please refer to Section1.2 for general discussion of this topic.

5.2 Selection of Critical Toxicity Study Endpoints for RiskAssessment

5.2.1 Acute ToxicityWe are concerned that the acute NOAEL selected by EPA is too high. CA DPR noted an acuteendpoint of 10 ppm from the rat study listed by EPA in Table 1 on page 21 of the 1,3-Dichloropropene Human Health Risk Assessment for Phase 2; DB Barcode D318784. No furtherdetails about this study (the dominant lethal assay for inhalation in rat) are provided by EPAeither in this section or in Appendix C. Please provide a description for this study and anexplanation for why this NOAEL was not used as the critical endpoint for acute toxicity. ThisNOAEL of 10 ppm is substantially lower than the 454 ppm NOAEL selected by US EPA, and norationale is provided for the selection of 454 ppm over 10 ppm. We recommend that 10 ppm beused as the more health-protective critical endpoint for acute toxicity. Our recommendation onthe use of this study may change if EPA provides the requested additional information.

Even considering the 454 ppm NOAEL, contradictions exist in US EPA’s discussion of thecritical endpoint selected for acute toxicity. In the Executive Summary of 1,3-DichloropropeneHuman Health Risk Assessment for Phase 2; DB Barcode D318784, 454 ppm is listed as theNOAEL and 583 ppm is the LOAEL; however, in Appendix B in the same document, in the HECArray table, the LOAEL is listed as 454 ppm and the NOAEL is listed as “Not identified”. Inaddition, the document indicates some undescribed percent mortality was observed for the647 ppm dose group and 100% mortality was observed in the 771 ppm dose group after 14 days.It seems unusual that no effects were observed at 454 ppm, a dose that was only 25% lower than adose that killed 100% of the test animals. If the dose-response curve is indeed that steep, anuncertainty factor of 30X is inappropriately low and a UF of at least 100X should be utilized.


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5.2.2 Developmental ToxicityWe are concerned that dosing in the critical developmental study occurred only on days 6-18 ofgestation, which does not provide information on adverse effects that may occur in the humanequivalent of the first trimester, the time period of greatest sensitivity for fetal development.

5.2.3 Subchronic (Intermediate) ToxicityPlease explain in more detail why the HEC of 5.0 ppm from the developmental toxicity study inrabbits was used instead of the dominant lethal study assay HEC of 2.5 ppm. The explanationgiven, that “the lower HECs identified in the dominant lethal assay appear to be an artifact ofdose selection/dose spread . . .” is not sufficient. Studies frequently give slightly different results,but lower values cannot be dismissed merely because a different study showed a different result.EPA’s job is to protect public health and, with that mandate in mind, the lowest critical endpointavailable from any valid study should be used.

5.2.4 CarcinogenicityEPA is underestimating the cancer risks from use of 1,3-dichloropropene. Rural residents wholive near fields fumigated annually with 1,3-D sustain high exposures over short periods of time.In addition, people living next to a field that is also in an area of generally high 1,3-D use willexperience lower level exposures throughout the fumigation season in their geographic area thatwill contribute to cancer risk.

EPA is to be commended for its inclusion of the CARB long-term monitoring data, but should beaware that California’s township caps and other use restrictions for 1,3-D were in effect when thismonitoring took place. Under these conditions, EPA’s exposure estimates are not accurate forother states where there are no such restrictions. Another factor contributing to the underestimateof cancer risks from 1,3-D is that the CARB monitoring cited in the risk assessment wasconducted in Kern, Santa Cruz and Monterey counties, which are not the highest areas of 1,3-Duse (see Figure 5-1).67 Also, as of 2003, use of 1,3-D has increased 75% since the CARB studieswere done in 2000 and 2001 (see Figure 5-2).

Figure 5-1: Use of 1,3-D is highest in Merced County, the central part of the Central Valley.Monitoring studies were conducted in the southern part of the Central Valley and in coastalMonterey County where use is lower, thus the monitoring data provide a low-end estimateof chronic exposure.


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0

1

2

3

4

5

6

7

8

1995 1996 1997 1998 1999 2000 2001 2002 2003

Use of 1,3-Dichloropropene in California 1995–2005

Mill

ions

of p

ound

s

Year

Figure 5-2: Use of 1,3-D has increased substantially since the monitoring studies cited byEPA were conducted in 2000 and 2001, thus current exposures can reasonably be expectedto be higher.

Thus, EPA’s conclusion that their assessment is representative of high-end exposure is notcorrect. The upper end cancer risks are likely to be higher than predicted by EPA, and the numberof people exposed to levels above the unit risk are higher than estimated by EPA. As we move tothe risk mitigation phase, we remind EPA that lifetime exposure is not to exceed a one-in-a-million increased lifetime risk.68

Several additional points/corrections should be included in EPA’s risk assessment.• Annual average exposure levels are typically used to estimate lifetime exposure risk.

However, for some chemicals, cancer risks at a given level of average annual exposurecould be much greater when exposures occur at higher levels for shorter durations, suchas exposures for near neighbors during a fumigation.69 This phenomenon has beendemonstrated in a study of 1,3-butadiene by the National Toxicology Program.70

• A recent study found elevated rates of pancreatic cancer in long-term residents in areas ofCalifornia with high 1,3-D application rates.71

• It seems as if there is a mistake in the units on the Q1* on page 23 and in Table 1 of 1,3-Dichloropropene Human Health Risk Assessment for Phase 2; DB Barcode D318784,which are showing up as “g/m3” and probably should be “µg/m3”. This may be a fontissue, in which case including all fonts in the pdf file would fix this problem.

• Please provide an explanation for why the Q1* was modified in 1997 and what value ofQ1* was used prior to that date.

• Please show the calculation for the determination of the Q1* and convert this value to anair concentration equivalent to unit risk.

5.3 Metabolism StudiesOverall, there is a lack of clarity and detail provided in the metabolism section of the riskassessment. This section contains subjective and non-scientific language and terminology.Specifically in section 3.3 (p. 16) of the Human Health Risk Assessment for 1,3-D, the


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pharmacokinetics of 1,3-D are discussed; however, no quantitative information is provided thatwould enable a scientific evaluation of the study data. For example:

• “Following oral administration, most of the radio label was found in the stomach andgastrointestinal tract with lesser amounts in the kidneys, liver . . . .”Please give actual percentages. How much is “most”? What do you mean by “lesseramounts”.

• “Dose-related increases in macromolecular bindings were noted in several organs withthe highest binding sites found in the non-glandular stomach.”Please clarify. In which organs besides the non-glandular stomach are effects observed?

• “In another study . . . adminatration of 1,3-D for14 days results in rapid absorption fromthe gastrointestinal tract with distribution to all tissues examined.”Please define “rapid” in terms of hours/minutes/days and list which tissues wereexamined.

• “There was rapid elimination in the urine, as carbon dioxide in expired air and smallamounts in the feces.“Please define “rapid” in terms of hours/minutes/days and provide the percentages of 1,3-D excreted via the different routes.

• “Nine metabolites were isolated from urine with two being identified as 1,3-D-mercapturic acid and sulfoxide derivative.Please clarify: The sulfoxide derivative of what molecule? Are you referring tomercapturic acid or one of the other metabolites? Please identify the other sevenmetabolites.

Without the numbers and complete descriptions of metabolites to fully characterize the effectsand time frame of the pharmacology, these study descriptions are of virtually no scientific value.

5.4 Dermal Exposure Risk AssessmentAccording to both US EPA and CDPR, 1,3-D is highly toxic by both the dermal and ocular routesof exposure (Toxicity Category I). However, based on a flawed assumption that one or both ofthese exposure routes would not be expected for humans, a risk assessment for dermal/ocularexposure was not included in the assessment. There are enough occurrences of spills and wholebody exposures described in the 1,3-D incident reports to warrant a risk determination viadermal/ocular exposure. We urge US EPA to include this analysis in the risk assessment,especially for workers. Furthermore, an aggregate exposure/risk assessment must include dermalexposures along with all other routes of exposure.

5.5 Uncertainty FactorsIn general, the discussion and justification for the use of uncertainty factors in the 1,3-D riskassessment is difficult to follow and the rationale for selecting uncertainty factors so unclear as toappear as if US EPA’s decisions were subjective and arbitrary. We recommend that US EPAadopt the more widely used and recognized methodology in risk assessment for deriving levels ofconcern for humans from toxicity data. That is, dividing NOAELs by factors of ten (or factors ofthree only when adequate data and scientific support are available and a complete discussionprovided) to correct for interspecies and intraspecies variation, converting LOAELs to NOAELs,and for addressing adequacy or uncertainty in the database.


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5.6 Cumulative Risk Assessment: 1,3-D Plus ChloropicrinChloropicrin is combined with 1,3-dichloropropene as a warning agent and also as an activeingredient. Chloropicrin is used with 1,3-D in various products at ratios varying fromapproximately 1:400 to 2:3. US EPA should include a discussion of the public health dataregarding chloropicrin/1,3-D formulations in its risk assessment. We have provided generalcomments regarding US EPA’s methods to evaluate cumulative risks of the soil fumigants insection 1.5. It is essential that US EPA quantify the health risks of the exposure to thecombination of 1,3-D and chloropicrin, including a complete toxicological evaluation ofcombined toxicity, exposure, and interaction between chloropicrin and 1,3-D to address the risksof using these the formulations.

When US EPA completes its assessment for chloropicrin as an active ingredient, we believe thatthe findings will demonstrate that chloropicrin is much more acutely toxic than 1,3-D. Therefore,we believe that the effects of chloropicrin, and not 1,3-D will dominate the acute toxicity hazardfrom the use of chloropicrin/1,3-D mixtures.

In looking toward the future for assuring worker and public health and safety related tofumigants, we remain concerned about the absence of regulatory controls specific to chloropicrin,an agent with high acute toxicity, and chloropicrin used in combination with 1,3-D and otherfumigants. Some registered 1,3-D products currently contain up to 60% chloropicrin, therebyincreasing our concern regarding this agent. Since products containing chloropicrin are being re-evaluated for registration purposes at this time, it seems appropriate and timely that US EPAinitiate rule making for this agent as it used in combination with other soil fumigants, in particular1,3-D and methyl bromide. We believe that when assessed together, the combination of thetoxicity levels of concern and the exposure risks for residents and workers will require even morestringent mitigation and control measures than the use of either of these chemicals alone. It isquite possible that the data will demonstrate that there is no safe means to handle mixtures of 1,3-D and chloropicrin.

5.7 Aggregate Risk AssessmentIt is not clear what approach US EPA has taken in deriving aggregate risks for 1,3-D. However,the document does not present a useful characterization of risks from exposure multiple exposureroutes. Therefore, the risk assessment is incomplete in this regard. Most likely, inhalation riskswould dominate an aggregate risk assessment, especially for subchronic and chronic toxicity.Dermal exposure is especially critical for acute exposures in workers, but was completely ignoredby US EPA. We recommend the authors revise the risk assessment document to include a fullquantitative analysis of all three exposure routes and all four exposure sources and provide a tableshowing aggregate risks for acute, subchronic and chronic exposure to 1,3-D.

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6 Metam Sodium and Dazomet Toxicology

6.1 Choice of NOAELs

6.1.1 Metam Short-Term Dermal NOAELThis risk assessment sets the metam sodium short-term Dermal NOAEL at 4.22 mg/kg based ondevelopmental toxicity in maternal rats where reduced weight gain and reduced foodconsumption was noted at a LOAEL of 16.88 mg/kg. In contrast, California DPR, with theconcurrence of OEHHA, is using a more health protective NOAEL of 1 mg/kg based onincreased early resorptions at 4.2 mg/kg in a rabbit study.72 The Agency should use this moreprotective NOAEL.

6.1.2 MITC Short and Intermediate-Term Effect LevelThis risk assessment sets the MITC short and intermediate term inhalation HEC at 160 ppb fornon-occupational and 680 ppb for occupational exposures based predominantly on the no effectslevel of metaplasia of the respiratory epithelium, with consideration of nasal epithelial atrophy.We are concerned that the agency here also has utilized a total uncertainty factor of 30 rather than100, with no studies cited to support this action. The use of an uncertainty factor of 100 is anestablished practice for the EPA and should be utilized for MITC.

In contrast, California DPR’s MITC intermediate or seasonal effect level,73 approved byCalifornia’s Toxic Air Contaminant Act Scientific Review Panel, is more health protectivebecause it is based on the estimated no effects level of 100 ppb for nasal epithelial atrophy andutilizes a total uncertainty factor of 300 for intra and inter-species variation (100x as isestablished practice) and 3x for extrapolation from a LOAEL to a NOAEL (as is establishedpractice). Since this subchronic NOAEL was based on the irritation endpoint of nasal epithelialatrophy, there was no need for systemic dose calculations or differentiation between occupationaland non-occupational endpoints. The Agency should adopt this methodology and intermediateMITC effect level used by DPR.

6.1.3 MITC Acute Inhalation Effect LevelWe note that the Agency has decided to adopt an acute (1-8 hour) inhalation effect level of 22ppb which is harmonized with DPR’s acute inhalation effect level. The need for a healthprotective acute effect level is strongly supported by the vast number of reports of eye andrespiratory irritation related to bystander exposure to MITC drift.

We support the Agency’s decision to use eye and respiratory irritation health effect endpointsbecause we agree that California pesticide illness data demonstrates that the general public isexposed to metam sodium decomposition products in air following application.

We support the concept that in the absence of more robust dose-response data from acuteexposures, eye irritation can be considered as a biomarker and surrogate for potential respiratoryeffects. However, we urge the Agency to utilize an additional uncertainty factor of 3 or 10 to


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estimate a NOAEL for respiratory effects due to the uncertainty of extrapolating from eye torespiratory effects, increased sensitivity of asthmatics, lower eye irritation NOAEL seen in catsand limitations of existing toxicology database, which are described in detail in the followingsubsection.

We are also uncomfortable with the fact that this acute (1-8 hour) inhalation effect level of 22 ppbwas set based on results of a human experimental exposure study. In general we oppose theconduct of this type of study because researchers cannot realistically provide adequateinformation for informed consent when they are doing a study to determine a NOAEL – sincethey don’t know all the potential effects the exposure could cause. Furthermore, people withlimited economic options will always have more incentive to “volunteer” for such studies. Also,such tests are often of limited scientific value in assessing risk to sensitive subpopulations,because human studies cannot ethically be conducted on the populations of greatest concern:children, infants, fetuses, and pregnant women, nor can they be conducted on numbers that wouldprovide any statistical power for evaluation of low-incidence adverse effects. Most concerning isthe fact that the study resulted in considerable pain and discomfort to its subjects, and therebyalso demonstrated,the need for a more protective acute exposure limit than the existing databaseof inhalation toxicology studies provides. EPA should require additional appropriate non-animalor animal studies to clarify the acute toxicity endpoint.

6.1.4 Limitations of Acute Inhalation Toxicity Studies for MITCHuman health risks for MITC are estimated in the risk assessment for acute inhalation exposuresbased on the eight-hour NOAEL of 220 ppb for eye irritation based on subjective symptoms ofeye discomfort at the next higher level of 800 ppb MITC.74 US EPA and CDPR73 used thisNOAEL for estimating levels of concern by dividing the NOAEL by an uncertainty factor of tento account for intraspecies variation. Prior to 1996, a NOAEL of 35 ppb for irritation of the ocularmucosa in a four-hour MITC exposure in cats75 was considered the most sensitive endpoint anddose for use in risk assessment by the Office of Environmental Health Hazard Assessment(OEHHA), including the 2002 evaluation of human health risks following the accidental spill ofmetam sodium into the Sacramento River at the Cantara Loop in 1991.76 Both the humanvolunteer study and the laboratory study in cats have limitations for use in quantitative riskassessment. These limitations are listed below for comparison:

Nesterova, 1969

The published report lacks essential information on experimental conditions and parameters:

• There is no information about the number of animals, sex, weight, or age of the threespecies reportedly used in the inhalation experiment.

• No control groups were specified.• It is not possible to determine whether the toxic effects seen in experimental animals

were based solely on MITC exposure:• The experimental method specified that MITC was generated from the decomposition of

metam sodium promoted by heated soils.• Measurements of airborne MITC were undertaken, but no measurements were made of

other volatile degradation products of metam sodium.• It is possible that toxic effects were due to the additive/synergistic effects of degradation

products with MITC, or to MITC itself.


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• The quality or accuracy of the MITC assay method is not described. No information wasprovided about the nature of the airborne concentrations, whether they were consistent orvariable, or when the measurements were undertaken.

• The effects reported were primarily clinical observations. There was no evidence for anextensive toxicity evaluation as would be conducted under FIFRA guidelines. No organweights or histology was reported, but some clinical chemistry and hematologyapparently were done (no specific tests were identified and only the results werereported).

Russell and Rush, 1996

This study attempted to determine the human eye irritation threshold using an eye mask. It did notaddress MITC effects on the upper respiratory tract or other parts of the human body.The recruitment questionnaire asked about medical history including eye infection/irritation,asthma, allergies, medication, smoking, and pregnancy. Subjects wearing contact lenses orpregnant and lactating women were excluded. However, the interim report did not indicate thenumber of subjects with the other noted conditions who were included in the study. For example,the study may have excluded subjects with asthma or hay fever, as they may not have wanted toparticipate in a study involving chemical irritants. Therefore, only healthy, young adults mayhave been represented.

The study included 138 human subjects (69 of each gender) recruited from the campuscommunity, with a mean age of 32 (range of 18 to 67). These subjects did not represent the fullage range or, probably, the racial make-up of the general population.

Lacrimation (tearing) may occur via the trigeminofacial reflex from either a direct (eye) orindirect (nasal) stimulation. By isolation of ocular from nasal exposure with the eye mask, theorigin of the reaction can be differentiated. However, most individuals would experience full-faceexposure to MITC with combined effects on nasal, eye, and upper respiratory nerve endings, andthe skin. The study does not provide data to assess this likely exposure scenario.

In animals, the Draize eye irritation test is evaluated using “irritation scores.” In the human study,a noninvasive, subjective approach is used. Each test subject is asked to report on perceived eyeirritation. Eye photographic analysis was found “not of value” because the more sensitiveindividuals “tended to be canceled out by others who displayed some native edema and redness inthe early morning.” It is unclear why this would not be useful, with each person acting as his orher own control, as stated. If this measure were applied properly, the results should have beenmore comparable to the animal irritation study method.

While the use of the human study for eye irritation over the experimental study in cats might bejustified, it should be noted that a human equivalency level based on the NOAEL from the catstudy would be significantly lower, and the MOEs significantly less, than those calculated in riskassessment using the human exposure study.

The critical acute endpoint of eye irritation used for evaluating acute human exposures to MITCwas from a human volunteer study where only the eyes were exposed (using goggles) to thematerial. In an actual exposure situation, the respiratory tract would be simultaneously exposed,which is very likely to lower the NOAEL for this endpoint. Uncertainty exists as to what degreethe NOAEL would be affected by this study design flaw. Furthermore, in practice, people aremost frequently exposed to airborne MITC following agricultural metam sodium applications.


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Under such conditions, inhalation exposure is not limited to MITC but also may include otherdegradation products such as methyl isocyanate, hydrogen sulfide, carbon disulfide, methylamineand formaldehyde. Uncertainty exists as to the degree of contribution of these products to theoverall potential toxicity.

Perhaps most importantly, uncertainty also exists as to the potency of MITC as a human dermaland pulmonary sensitizer. Potential sensitization properties of airborne MITC following metamsodium applications might also be enhanced due to methyl isocyanate co-exposures. No sensitivesubpopulations have been specifically identified in US EPA’s risk assessment, although it hasbeen observed that people with pre-existing respiratory conditions can be especially vulnerable tochemicals with respiratory irritant and sensitization properties (including reactive airwaysdysfunction syndrome, or RADS).77 The occurrence of RADS has been well documented inCalifornia following high-level MITC exposures from accidental releases and agricultural uses ofmetam sodium. In particular, OEHHA describes such episodes in its 1992 risk assessment of themetam spill in the Sacramento River. It should be noted that human complaints of respiratory andeye irritation occurred at lower doses than those reported in the 1996 human volunteer study. Infact, the levels of concern derived from air sampling and human symptoms were comparable withthe levels that caused lacrimation in cats.78

We recommend that US EPA include a summary of the OEHHA risk assessment because itrelates specifically to uncontrolled human exposures of MITC at levels that might be expectedfollowing metam application in agricultural fields.79 In addition, because of the significant levelof uncertainty surrounding the acute toxicity data, the reports and quantitative analysis ofuncontrolled human exposures, and the well-documented susceptible human subpopulation ofasthmatics, an additional uncertainty factor of 3 to 10 should be applied to the human volunteerdata for a total of 30 or 100-fold uncertainty factor.

6.2 Use of Uncertainty Factors/FQPA Factor/MOEs

6.2.1 FQPA FactorWe dispute the conclusion that metam sodium does not need to be considered under the FoodQuality Protection Act (FQPA) because it does not pose food residue concerns. Ambient airmonitoring conducted in California found that exposure to MITC from multiple metam sodiumapplications occurred on the vast majority of days during the entire six week monitoring period atseveral Kern county schools used as monitoring sites (ARB 2003). It is well documented thatchildren are exposed to MITC when it drifts into residential areas and have suffered new andaggravated cases of asthma as a result. As such, this drift to non-workers needs to be consideredunder FQPA standards since FQPA requires consideration of all non-occupational exposures.

6.3 Additional Issues

6.3.1 Failure to Consider Cumulative Exposure to other DegradationProducts

We share the Agency’s conclusion that exposure to metam sodium and dazomet’s otherbreakdown products (methyl isocyanate, hydrogen sulfide, carbon disulfide, methylamine andformaldehyde) are also of toxicological concern to workers and bystanders. We feel that theagency should estimate inhalation exposures to these additional breakdown products and assesstheir combined health impacts, particularly since both methyl isocyanate and hydrogen sulfide


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also act primarily on the eyes and respiratory system and concurrent exposure could exacerbatethe development of asthma and other reactive airways disorders.

6.3.2 Metam Sodium Field Monitoring Should Not Require ChemicalInhalation

California labels and permit conditions require compliance with a Technical Information Bulletin(TIB) developed by the metam sodium manufacturers. This TIB requires monitoring every hourfor air and soil temperature, wind direction and odor during and 12 hours post-application for allsoil fumigation methods. In our view, hourly monitoring of soil and air temperature and winddirection is worthwhile as long as the employee conducting the monitoring is supplied withappropriate, effective eye and respiratory protection. Many drift poisoning incidents have resultedafter wind changed direction and the temperature changed, signaling development of inversionconditions. However, we share the conclusion of California Department of Health ServicesOccupational Health Branch that odor detection as a field monitoring practice for metam-sodiumis not health protective and is not a reliable warning method for an acute health hazard. (DHSOHB 2001) Odor detection is not a reliable warning method, because, as detailed in the DHSreport, the odor threshold of metam sodium ranges between 200 and 8,000 ppb amongindividuals. Estimated one-hour MITC exposure levels to prevent acute respiratory and eyeirritation symptoms (22 ppb and 0.5 ppb) are nine and 400 times less than the lowest odorthreshold (DHS OHB 2001). If the use of MITC-generating chemicals is to continue, there is anurgent need to develop a sensitive and reliable method to measure MITC levels instantaneouslyand to refine use restrictions to better contain metam sodium and its breakdown products on site.

6.3.3 MITC and Dazomet Data Gaps Are AlarmingWe are extremely concerned about the numerous MITC toxicology data gaps and conclude thatuse of metam sodium and dazomet should not be allowed to continue with the many gaps in ourknowledge of potential short and long-term effects of MITC exposure. The industry has alreadyhad many years to fill these data gaps. We concur with the conclusions expressed by the Agencythat inhalation carcinogenicity studies in rats and mice and an acute inhalation neurotoxicitystudy in rats including pathological evaluation of the upper and lower respiratory tract are neededfor MITC. The Agency should request initiation of these studies without further delay andprohibit all uses of MITC-generating chemicals until the data are received.

6.3.4 Summary does not Accurately Characterize Metam SodiumIllness Reports

The poisoning incident summary only mentions metam sodium illnesses for California through1997 while details of the risk assessment summarize incident reports through 2003. The incidentsummary should include statistics on illness reports through 2003.

6.3.5 Metam Sodium (MITC) Monitoring Studies UnderestimateBystander Exposure

This risk assessment and a previous draft80 utilized a single study for each application method tocharacterize off-site exposures exceeding a level of concern at specific distances from the field.Acute and Short-term air levels with inadequate MOEs were recorded at the maximum distancemonitored (1,000 feet), for both sprinkler and shank applications with standard water seals and at274 and 300 feet respectively for sprinkler and shank applications with intermittent water seals.These results are particularly disturbing given that the industry sponsored studies chosen for


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sprinkler and shank standard water seal methods underestimate exposure as explained below.This draft risk assessment also fails to adequately characterize the weaknesses and limitations ofthese studies.

Study Weaknesses and Limitations

Study 457037-01 conducted by the Metam Sodium Task Force in Kern county in summer of 1999did not position samplers evenly around the field. Consequently, when the wind changeddirection during the study there were no samplers located in a downwind direction during asignificant portion of the study. For this reason, the California Department of PesticideRegulation has concluded that MITC concentrations obtained from this study are likelyunderestimated. We agree.

Study 457037-02 conducted by the Metam Sodium Task Force in Kern County in the summer of2001 only positioned samplers to the southeast and southwest of the field at 274 meters andbeyond. While prevailing winds were reported to come from the north and northwest, maximumdownwind MITC concentrations were not necessarily captured at 274 meters and beyond becausethere was undoubtedly some fluctuation in the wind direction.

Study 457037-04 conducted by the Metam Sodium Task Force in Kern County in summer of2001 did not position samples evenly around the field at the 500 m and 700 m distances and winddirections were not reported for this study so there is no way of ascertaining whether or not MITCconcentrations were underestimated at 500 m and 700 m from the treated field. Withoutinformation on the direction of prevailing winds, the study should be rejected.

Study 457037-08 conducted by the Metam Sodium Task Force in Orange County in the winter of1997 was not conducted under worst case weather conditions and sampling stations at 6.1 metersand further from the field were only located to the north and northeast and wind directions werenot reported so there is no way of ascertaining whether or not MITC concentrations wereunderestimated at and beyond 6.1 meters from the field. We recommend increasing buffer zonesto compensate for this weakness

We also request that EPA include the many exposure monitoring studies conducted by theCalifornia Air Resources Board (CARB), an organization that has no conflict of interest inobtaining accurate and representative exposure monitoring data for a variety of applicationmethods and conditions. We summarize some of these studies in Table 6-1 below and compareand contrast them to selected industry studies. Note that only certain ARB studies provide trulyrepresentative data. All industry studies suffer from misplacement of monitoring stations suchthat the true worst-case scenarios were not captured.


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Table 6-1: Comparison of MITC Application Site Monitoring Studies81

Date andLocation

MonitoringConducted

ByApplication

Type

ApplicationRate

(lbs AI/acre)Acres

Treated

Distance toField

Border(feet)

MaximumConcentration

at Distance(ng/m3)a Comment

Aug-93Kern Co.

DPR sprinkler 318 20.0 488 3,946,800 Representative of worst-caselegal scenario: high applicationrate, high temperatures, sprinklerapplication. Good quality data.

Jun-99Kern Co.

Merricks sprinkler 320 80.0 488 839,000 High application rate, hightemperatures. Maximummeasured concentration is not atrue maximum, since few or nosamplers were placed directlydownwind.

Jun-99Kern Co.

Merricks soilinjection

320 79.0 488 839,800 High application rate, hightemperatures. Maximummeasured concentration is not atrue maximum, since few or nosamplers were placed directlydownwind.

Aug-95Kern Co.

ARB soilinjection, nosealing

155 80.0 39 250,000 Intermediate application rate,high temperatures, no sealing.Maximum measuredconcentration is not a truemaximum, since no samplerswere placed directly downwind.

May-92MaderaCo.

Rosenheck sprinkler 305 6.7 406 856,000 High application rate, lowtemperatures. Maximummeasured concentration is not atrue maximum, since samplerswere positioned perpendicular towind direction

Mar-93ContraCostaCo.

ARB soilinjection, nosealing

57 95.0 45 242,000 Representative of best-casescenario with no soil sealing.Low application rate, lowtemperatures. Good quality data.

Jul-93Kern Co.

ARB soilinjection,sealedb

155 85.0 60 880,000 Intermediate application rate,high temperatures, soil sealed.

*Source:Evaluation of Methyl Isothiocyanate as a Toxic Air Contaminant, California Department of PesticideRegulation, August 2002, http://www.cdpr.ca.gov/docs/empm/pubs/tac/finlmenu.htm.a. Maximum concentrations were chosen for distances that were as comparable as possible across the different

studies, and do not necessarily represent the maximum concentration observed for the entire study.b. DPR's summary of CARB's study indicated the soil was not sealed; however, in an errata note attached to the

original monitoring report, CARB indicates the soil was sealed.

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7 US EPA Must Seriously Consider Existing ViableAlternativesIn the document entitled “Overview of the Use and Usage of Soil Fumigants,” soil fumigantalternatives are mentioned and quickly dismissed. The document reaches the conclusion that thedifferent fumigants are alternatives to each other, and non-fumigant control measures all haveunacceptable trade-offs. We are concerned that EPA is ignoring the many viable alternatives thatare available and the ongoing research that will make more non-chemical methods of soil pestcontrol available in the future. UNEP’s Methyl Bromide Technical Options Committee(MBTOC) has been compiling alternatives to methyl bromide for many years. The otherfumigants also have viable alternatives available and under development. These alternatives allowfor safer practices and continued profits. The following section highlights a few of these options.We would like to emphasize that the examples described below are only highlights of theinformation available. In order to do an accurate cost-benefit analysis, EPA must take thealternatives seriously and do a comprehensive evaluation of them as viable options to the use offumigants.

7.1 Percentage of Crops Treated with Soil FumigantsAn analysis of the “Overview of the Use and Usage of Soil Fumigants,” shows that farmers aregrowing these crops, even those traditionally the most fumigant intensive, without the use ofdangerous fumigants. Table 2 of the Use and Usage document presents the pounds of fumigantsused and the percentage of crop being treated for the highest use crops. Table 7-1 in this commentletter is a reproduction of Table 2 with two additional columns showing the total percent croptreated with any fumigant and the percentage of the crop grown without fumigants. The first graycolumn is the sum of the percentage of crop treated by the four individual fumigants. If, in agiven year, 27% of the potato crop is treated with fumigants, then 73% of the crop is being grownwithout fumigants. Even strawberry production, with the highest percentage of the crop treatedwith fumigants, still has 24% of crop not being treated by fumigants. Because the fumigants areoften used together on a single field, the sums of the percentages treated is probably even lowerthan the calculated values, making the percentages of the crops using alternate methods evenhigher than those presented in Table 7-1. These numbers indicate that farmers can grow thesecrops, even those typically most fumigant intensive, without the use of dangerous fumigants. TheEPA needs to do a serious analysis of these methods of pest control during phase 5 of the riskassessment and not assume, as it has, that fumigants are necessary to grow crops.


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Table 7-1: Reprint of Table 2 in “Overview of the Use and Usage of Soil Fumigants” withAdditional Columns (Gray) Totaling the Percentage of the Crop Treated (PCT) with AnyFumigant and the Percentage of Crop Not Treated

*Calculated by adding the four individual fumigant PCT values. Values of <1 were considered to be 1.

7.2 US EPA Must Consider the External Costs of Fumigant UseEPA needs to perform an accurate and balanced economic analysis of the costs and benefits of thesoil fumigants, factoring in the external costs to the environment and human health. In thedocument entitled “Overview of the Use and Usage of Soil Fumigants,” one of the tradeoffs ofswitching to non-chemical alternatives mentioned by EPA is the increased cost of these methods.EPA seems to be going to great lengths to estimate the costs of the alternative methods, includingasking questions of farmers about the costs of eliminating fumigants from their pest-controlstrategies. However, EPA has taken no initiative to evaluate the external costs of the continueduse of soil fumigants discussed, including illnesses and environmental degradation. Although theEPA has not preformed a complete cost analysis in the cluster assessment documentation, itpresumes higher costs for non-chemical alternatives and uses this as a factor in favor of the use ofthe soil fumigants. For an accurate cost-benefit analysis, EPA needs to consider the external costson the environment and on the health care system of the continued use of fumigants

There are several studies available that estimate the external costs of pesticide use. While notspecific to fumigants, they do give some idea of the magnitude of the external costs and why theyneed to be considered in the risk assessment process. According to a 2004 study at Iowa StateUniversity, the estimated external costs of agricultural production in the United States annuallyranges from $5.7 to $16.9 billion dollars.82 Of these costs, $2.3 billion are related to pesticidedamage and control methods. Of this pesticide-related amount, $1.01 billion (adjusted forinflation from the original 1992 numbers) is attributed to health costs of pesticide poisonings.83

Chloropicrin Metam Sodium Methyl Bromide 1,3-Dichloropropene

Crop Pounds PCT Pounds PCT Pounds PCT Pounds PCT Total PoundsPCT with soil

fumigants*

PC usingalternatecontrol

methods

Potatoes 200,000 <1 31,700,000 20 200,000 <1 9,900,000 5 42,000,000 27 73

Tomatoes 1,700,000 10 7,000,000 15 10,600,000 20 300,000 5 19,600,000 50 50

Tobacco 3,600,000 15 100,000 <1 500,000 <1 7,800,000 10 12,000,000 27 73

Carrots 70,000 <1 9,000,000 40 70,000 <1 1,500,000 10 10,640,000 52 48

Strawberries 1,400,000 20 200,000 <1 7,600,000 50 400,000 5 9,600,000 76 24

Peppers 700,000 10 700,000 5 3,700,000 20 200,000 5 5,300,000 40 60

Watermelons 800,000 <1 700,000 2 2,300,000 5 400,000 <1 4,200,000 9 91

Onions 200,000 <1 1,700,000 5 200,000 <1 900,000 5 3,000,000 12 88

Cucumbers 100,000 5 300,000 <1 1,300,000 5 900,000 10 2,600,000 21 79

Peanuts 5,000 <1 1,100,000 5 1,300,000 <1 2,405,000 7 93

Cantaloupes 100,000 5 800,000 5 800,000 5 300,000 5 2,000,000 20 80

Sweet Potato 100,000 6 300,000 1 800,000 5 800,000 20 2,000,000 32 68

Squash 80,000 <1 100,000 1 400,000 5 200,000 5 780,000 12 88

Cabbage 60,000 <1 200,000 5 260,000 6 94

Eggplant 6,000 <1 200,000 45 206,000 46 54

Celery 200,000 10 200,000 10 90

Artichokes 50,000 5 50,000 5 95

Brussels Sprout 60,000 30 60,000 45 120,000 75 25


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These numbers, relying on estimates about the number of illnesses and death, do not considermissed diagnoses (of which there are likely to be many), misdiagnoses and chronic illnesses otherthan cancers, and so are probably lower than the actual health care costs.

While the Iowa State University study did not specifically analyze fumigant use, it can reasonablybe anticipated that fumigants are significant contributors to the total costs because of their highacute and chronic toxicity and high use. Costs to public and environmental health from depletionof the ozone layer due to the continued use of methyl bromide and the costs of soil erosion andloss of soil water-retaining capacity as a result of fumigant use84 have been left out of theequation. A risk assessment that does not account for these significant costs is unscientific andunrealistic. EPA must include an accurate assessment of the true costs of fumigant use in its riskassessments for the fumigants.

7.3 Fumigant-Intensive Crops Can Be Grown Cost Effectivelywithout Soil Fumigants

Fumigants are not the only options for pest control in the production of conventionally high-fumigant-use crops. Farmers are growing these crops successfully without the use of soilfumigants and are doing so while making a profit. In this section, we provide some examples ofsuccessful non-chemical pest control methods now in use and currently under development. Thisis not meant to be a comprehensive summary, but to show that non-chemical soil pest control isbeing done successfully and is economically viable. We request that EPA include acomprehensive survey of non-chemical methods for soil pest control in its phase 5 riskassessment document.

7.3.1 Strawberries and TomatoesA number of approaches have been effective in strawberry and tomato cultivation to control theentire range of common pests without the use of fumigants or other toxic pesticides. Methodsinclude: rotating crops in the fields, planting cover crops, and soil solarization to controlpathogens and weeds, and mechanical cultivation of weeds. A Florida study performed by the USDepartment of Agriculture (USDA) showed that solarization, combined with deep disking priorto application of plastic tarpa, produced yields 23% greater than adjacent plots fumigated withmethyl bromide Farmers using cover crops reported better net profits than farmers growingtomatoes with conventional methyl bromide applications, due to savings on the costs of methylbromide and fertilizer.85

The University of California at Davis (UC Davis) studied two strawberry farms in the samegrowing region in California, a conventional farm using fumigants in 2004 and an organic farmusing alternate methods to control the same problems in 2003.86, 87 The conventional farm usedmethyl bromide and chloropicrin in a pre-plant fumigation to control weeds, nematodes, andother soil-borne pests while the organic farm used less toxic methods to control the same pests.Table 7-2 shows the results. Organic strawberry farming produced higher yields per acre, butrequired more labor for hand weeding and disease control; therefore the organic farm’s cost peracre was higher (see Table 1-2). In the end, both methods were profitable and the relatively smallprofit difference (5.4%) between the two methods is far outweighed by the significantenvironmental and public health costs of fumigant use.


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Table 7-2: Organic and Conventional Strawberry and Tomato Comparison, based on UCDavis studies

Yield per Acre Cost per Acre Profit per Acre

Organic Strawberries 3,000-4,500 12 pound trays $10,400 $1,885

Conventional Strawberries 2500 12 pound trays $9,000 $1,993

Organic Tomatoes 28 tons $1,572 $527

Conventional Tomatoes 33.66 tons $1,710 $585

UC Davis conducted a similar of comparison of organic and conventional tomato farms inCalifornia’s Sacramento Valley.88, 89 In this study, conventional yields were higher, but so wereproduction costs. Overall net profits for organically grown tomatoes were only 10% lower thanconventionally grown tomatoes. The study results for tomatoes were similar tostrawberries—both methods can be profitable and, again, the relative difference in profits shouldbe evaluated in terms of both the price consumers will pay for cleaner production and the fargreater costs of damage to the environment and human health associated with the large-scalerelease of dangerous fumigants.

7.3.2 Potatoes and CarrotsPotatoes and carrots are the two crops using the most metam sodium annually and they both havehigh Telone usage as well. These fumigants are used to control many soil pests, but one that is ofprimary concern to potato and carrot farmers is nematodes.

Washington State University and the University of California, Davis Cooperative Extension havebeen experimenting with planting mustard as a cover crop, then disking it into the soil beforepotato and carrot planting. As it decomposes, mustard releases low levels of isothiocyanates(similar to MITC, one of the chemicals released by the use of metam sodium) havingbiofumigation effects that kill nematodes and other pest organisms in the soil. Mustard has theadditional benefit of soil enrichment as a “green manure” cover crop. Cover crops increase thewater filtration potential, organic matter, and general soil health of the fields leading to erosioncontrol.90 In a University of California, Davis Cooperative Extension study comparing mustardand metam sodium potato production, the total yield for potatoes grown with mustard wasslightly higher than those grown with metam sodium.91 This is not the case only in studies, but isbeing used on farms in place of metam sodium. A potato farmer in Washington State, who washaving trouble with soil productivity on his farm, switched some of his fields to mustard covercrops in place of applying metam sodium.92 Over a three-year period, he has seen the fields usingmustard perform just as well as the ones using metam sodium. He has also seen more than a 30%increase in the soil’s water holding capacity. According to the Agricultural Research Service inWashington, more research needs to be done to determine the exact mechanisms of biofumigationof the mustard plant.93 Additional research can optimize the use of mustard as a cover crop, andeven higher yields may be possible.


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In addition to the use of mustard as a natural fumigant and cover crop, carrot growers are usingseveral other methods of combating harmful pests. Several nematodes are very damaging tocarrot production. The California Fresh Carrot Advisory Board is dealing with the nematodeproblem by funding research to introduce traits into commercially grown carrot species fromwild-carrot cultivars from other countries in order to produce carrots resistant to harmfulnematodes and diseases.94 General integrated pest management (IPM) practices in the productionof carrots also help to curb the damage done by nematodes. The IPM program at UC Davisrecommends planting carrots at less than 64° F because three root-knot nematodes (M. incognita,M. javanica, and M. arenaria) are not active at that temperature.95

These cost-effective methods of pest control for tomato, strawberry, carrot, and potato crops arejust a few examples of the types of technologies that farmers are using to grow crops without theuse of toxic fumigants. There are many alternatives already in use by farmers growing otherwisehigh-fumigant-use crops in both large and small farming operations. The EPA should seriouslyresearch and consider these alternatives in light of the significant toxic health and environmentalimpacts of chemical fumigants.

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Endnotes 1 California Department of Pesticide Regulation Toxicology reviews are available electronicallyat http://www.cdpr.ca.gov/docs/toxsums/toxsumlist.htm.2 The Office of Management and Budget, “Guidelines for Ensuring and Maximizing the Quality,Objectivity, Utility, and Integrity of Information Disseminated by Federal Agencies” areavailable at http://www.whitehouse.gov/omb/fedreg/reproducible.html.3 A Review of the Reference Dose and Reference Concentration Processes, External ReviewDraft, EPA/630/P-02/002A, US EPA, May 2002, page 4-29.4 Memorandum: Soil Fumigant Assessment, Soil Fumigant Users Group, May 4, 2005.5 B. Johnson, Executive Summary of Report EH 00-10: Evaluating the Effectiveness of MethylBromide Soil Buffer Zones in Maintaining Acute Exposures Below a Reference AirConcentration, Environmental Monitoring Branch, Department of Pesticide Regulation,Environmental Protection Agency, State of California, EH 00-10, April 2001.6 Major pesticide poisonings in California are highlighted in the annual reports of the PesticideIllness Surveillance Program, available at http://www.cdpr.ca.gov/docs/whs/pisp.htm.7 M. O’Malley, T. Barry, M. Verder-Carlos, A. Rubin, Modeling of Methyl Isothiocyanate AirConcentrations Associated With Community Illnesses Following a Metam-Sodium SprinklerApplication, Am J Ind Med, 2004, 46:1-15.8 K.S. Goh, T. Barry, Estimation of Methyl Isothiocyanate Air Concentrations During the ArvinIncident, Memorandum, Department of Pesticide Regulation, State of California, November 8,2002.9 Pesticide Episode Investigation Report, Priority Investigation 33-RIV-03, PesticideEnforcement Branch, Department of Pesticide Regulation, State of California, December 3, 2003.10Final Report: Lamont Pesticide Drift: Emergency Preparedness, 2003-2004 Kern CountyGrand Jury, County of Kern, Superior Court of California,http://www.co.kern.ca.us/grandjury/fy0304/adminaudit.pdf.11 We used the US Naval Observatory Astronomical Applications Department calculator availableat http://aa.usno.navy.mil/data/docs/RS_OneYear.html which computes sunrise and sunset timesfor these locations in PST.12 A description of the CIMIS system and web forms that deliver weather data are available athttp://wwwcimis.water.ca.gov/cimis.13 See http://www.energy.ca.gov/daylightsaving.html. Beginning in 2007, this is not a validheuristic.14 Common cutoffs are those defined by (1) the Pasquill stability classes (less than 5 mph forstability classes E and F), (2) by a conventionally used

1 m/s, or (3) by a “calm and near-calm” range of 2 mph or lower.


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15 Land-based (surface) hourly weather data may be procured from the NOAA Satellite andInformation Service, National Climatic Data Center, http://www.ncdc.noaa.gov/.16 Consult http://lwf.ncdc.noaa.gov/oa/climate/rcsg/datasets.html for the TD-3280 stationinventory and data dictionary.17 Weather stations in TD-3280 datasets are identified by Weather Bureau-Army-Navy (WBAN)ID. These can be translated to other identifiers such as the International Civil AviationOrganization (ICAO) Location Indicator, or to a place name, by referring to the cross-referencetable at ftp://ftp.ncdc.noaa.gov/pub/data/inventories/WBAN.TXT.18 Obtained from http://www.air-dispersion.com/formulas.html.19 Guideline on Air Quality Models, EPA 40 CFR Ch. I (7–1–03 Edition) Pt. 51, App. W,available from US EPA Air Quality Modeling Group, Support Center for RegulatoryAtmospheric Modeling (SCRAM), http://www.epa.gov/ttn/scram/.20 AERMOD: Latest Features and Evaluation Results, Emissions Monitoring and AnalysisDivision, Office of Air Quality Planning and Standards, US Environmental Protection Agency,EPA-454/R-03-003, June, 2003, http://www.epa.gov/scram001/7thconf/aermod/eval.pdf.21 Steven Perry, Atmospheric Sciences Modeling Division, Air Resources Laboratory, NOAA,private communication regarding meander algorithm in AERMOD, October 12, 2005.22 A. J. Cimorelli, et al, AERMOD: A Dispersion Model for Industrial Source Applications, PartsI and II, J App Meteorology, 2005, 44:682-708.23 AERMOD: Latest Features and Evaluation Results, US EPA, Office of Air Quality Planningand Standards, EPA-454/R-03-003, June, 2003,http://www.epa.gov/scram001/7thconf/aermod/eval.pdf.24 A.J. Cimorelli, et al, AERMOD: A Dispersion Model for Industrial Source Applications. Part I:General Model Formulation and Boundary Layer Characterization, J App Met, 2005, 44:682-693.25 A.J. Cimorelli, et al, AERMOD: A Dispersion Model for Industrial Source Applications. PartII: Model Performance against 17 Field Study Databases, J App Met, 2005, 44:694-708.26 Soil Fumigants: Preliminary Risk Assessments Technical Briefing - July 13, 2005, Slide 97.The Technical Briefing is available athttp://docket.epa.gov/edkpub/do/EDKStaffCollectionDetailViewByID?collectionId=OPP-2005-0168.27 B. Johnson, T. Barry, & P. Wofford, Workbook for Gaussian Modeling Analysis of AirConcentration Measurements, State of California, Environmental Protection Agency, Departmentof Pesticide Regulation, EH99-03, September, 1999.http://www.cdpr.ca.gov/docs/empm/pubs/ehapreps/eh9903.pdf.28 Estimation of Exposure of Persons in California to Metam-Sodium During Soil Applications ofProducts Containing Metam-Sodium, California Department of Pesticide Regulation, HS-1703,Revision No. 1 June 24, 2004.29 Shelley Davis, Farmworker Justice Fund, private communication.30 K. Mehta, S.M. Gabbard, V. Barrat, M. Lewis, D. Carroll, & R. Mines (2000), Findings fromthe National Agricultural Workers Survey (NAWS) 1997-1998: A Demographic and


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Employment Profile of United States Farmworkers (Research Report No. 8), Washington, DC:US Department of Labor. Available at http://www.dol.gov/asp/programs/agworker/report_8.pdf.31 Review of Methyl Bromide Incident Reports, DP Barcode D283047, Chemical #053201, USEPA, May 30, 2002.32 Estimation of Exposure of Persons in California to Metam-Sodium During Soil Applications ofProducts Containing Metam-Sodium, California Department of Pesticide Regulation, HS-1703,Revision No. 1, June 24, 2004,33 California Code of Regulations, Title 3, Section 6738h.34 Title 29, Code of Federal Regulations, Section 1910.134.35 Cholinesterase Monitoring in Agriculture, WAC 296-307-148, Washington State Departmentof Labor and Industries, January 6, 2005.36 Evaluation of Charcoal Tube and SUMMA Canister Recoeries for Methyl Bromide AirSampling, California Department of Pesticide Regulation, Report EH 99-02, 1999.37 H. Fong, California Department of Pesticide Regulation, e-mail communication to A. Katten ofCRLAF, December 26, 2001.38 R.M. Hall, W.A. Heitbrink, & L.D. Reed, Evaluation of a Tractor Cab Using Real-TimeAerosol County Instrumentation, Applied Occupational and Environmental Hygiene, Volume17(1) 47-54, 2002.39 P.E. Newton, A four-week inhalation toxicity study of methyl bromide in the dog, 1994,Pharmaco LSR, Study Number 93-6068, CDPR Vol. 123-164 #132821.40 Methyl Bromide: Revised Health Effects Division (HED) Human Health Risk Assessment forPhase 3, US EPA, June 13, 2005.41 G. Schafer, A six-week inhalation toxicity study of methyl bromide in dogs, 2002, WILResearch Laboratories, Inc., 1407 George Road Ashland, OH 44805-9281, Study number WIL440001, CDPR Vol. 123-212 #187459.42 Methyl Bromide – 2nd Report of the Hazard Identification Assessment Review Committee, USEPA, HED Doc. No. 0051439, January 6, 2003.43 Summary of Toxicology Data: Methyl Bromide, California Department of Pesticide Regulation,January 2005, http://www.cdpr.ca.gov/docs/toxsums/pdfs/385.pdf.44 To obtain methyl bromide risk characterization documents and appendices from CDPR, go tothe Web site at http://www.cdpr.ca.gov/docs/dprdocs/methbrom/riskasses_fum.htm.45 To obtain documents regarding CDPR’s methyl bromide risk characterization documents andother related scientific analyses of methyl bromide and risk mitigation, go to the Web site athttp://www.oehha.ca.gov/pesticides/peer/petsmethylb.html.46 Methyl Bromide Risk Characterization in California: Subcommittee on Methyl Bromide,National Research Council, National Academy Press, Washington, D.C., 2000,http://www.cdpr.ca.gov/docs/dprdocs/methbrom/riskasses_fum.htm.47 OPPTS Harmonized Test Guidelines; Neurotoxicity Screening Battery, Office of Prevention,Pesticides and Toxic Substances, US EPA, 1998.(http://www.epa.gov/opptsfrs/OPPTS_Harmonized/870_Health_Effects_Test_Guidelines/index.html).


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48 OPPTS Harmonized Test Guidelines; 90-Day Inhalation Toxicity, Office of Prevention,Pesticides and Toxic Substances, US EPA, 1998.(http://www.epa.gov/opptsfrs/OPPTS_Harmonized/870_Health_Effects_Test_Guidelines/index.html).49 Comments on the Risk Characterization Document for Inhalation Exposure to Methyl Bromide,Addendum to Volume I, Prepared by the Department of Pesticide Regulation, Office ofEnvironmental Health Hazard Assessment, March 11, 2003,http://www.oehha.ca.gov/pesticides/peer/petsmethylb.html50 Methyl Bromide – 2nd Report of the Hazard Identification Assessment Review Committee, USEPA, HED Doc. No. 0051439, January 6, 2003.51 R.G.S. Reuzel, H.C. Dreef-van der Meulen, V.M.H. Hollanders, et al., Chronic inhalationtoxicity and carcinogenicity study of methyl bromide in Wistar rats, Food and ChemicalToxicology, 1991, 29:31-39.52 Methyl Bromide Risk Characterization Document, Volume I, Inhalation Exposure, CaliforniaDepartment of Pesticide Regulation, February 14, 2002,http://www.cdpr.ca.gov/docs/dprdocs/methbrom/rafnl/mebr_rcd.pdf.53 Methyl Bromide Risk Characterization Document, Volume II, Dietary Exposure, CaliforniaDepartment of Pesticide Regulation, February 21, 2002,http://www.cdpr.ca.gov/docs/dprdocs/methbrom/rafnl/vol2dietary.pdf.54 Methyl Bromide – Report of the FQPA Safety Factor Committee, US EPA, Health EffectsDivision, June 21, 2001.55 Pesticides in the Diets of Infants and Children, National Academy of Sciences, NationalResearch Council, National Academy Press, Washington, D.C., 1993.56 G.M. Calvert, G. Talaska, C.A. Mueller, et al., Genotoxicity in Workers Exposed to MethylBromide, Mutation Research, 1998, 417:115-128.57 S. Langard, T. Rognum, O. Flotterod, V. Skaug, Fatal accident resulting from methyl bromidepoisoning after fumigation of a neighboring house; leakage through sewage pipes, J. Appl.Toxicol. 1996, 16:445-448.58 E. T. Hallier, D. Langhof, M. Dannappel, et al., Polymorphism of glutathione conjugation ofmethyl bromide, ethylene oxide and dichloromethane in human blood: influence on the inductionof sister chromatid exchanges (SCE) in lymphocytes, Arch. Toxicol., 1993, 67 (3):173-178.59 H.H. Nelson, J.K. Wiencke, D.C. Christiani, et al., Ethnic Differences in the prevalence of thehomozygous deleted genotype of glutathione S-transferase theta, Carcinogenesis, 1995,16(5):1243-1245.60 R. Whalen, T.D. Boyer, Human glutathione S-transferases, Seminars Liver Disease, 1998,18:345-358.61 AA. Fryer, R. Hume, R.C. Strange, The development of glutathione S-transferase andglutathione peroxidase activities in human lung, Biochem Biophys Acta, 1986, 883:448-453.62 M.C. Alavanja et al., Prostate Cancer and Agricultural Pesticides, Agricultural Health Study,University of Iowa, 2003, www.aghealth.org.63 M. Alavanja, Samanic, C., et al.,Use of agricultural pesticides and prostate cancer risk in theAgricultural Health Study cohort, Am J Epidemiology, October 2002


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64 P. Mills and Yang, R. Prostate cancer risk in California farmworkers, Journal of Occupationaland Environmental Medicine, March 2003)65 EPA. 2005. Guidelines for Carcinogen Risk Assessment and Supplemental Guidance forAssessing Susceptibility from Early-Life Exposure to Carcinogens.http://cfpub2.epa.gov/ncea/raf/recordisplay.cfm?deid=116283.66 Schneider et al., Glutathione activation of chloropicrin in the Salmonella mutagenicity test,Mutation Research, 1999, 439:233-238.67 California Pesticide Use Reports, California Department of Pesticide Regulation,http://www.cdpr.ca.gov/docs/pur/purmain.htm.68 R. Castorina & T.J. Woodruff, Assessment of Potential Risk Levels Associated with US EPAReference Levels, Environ Health Persp, 2003, 111(10):1318-25.69 Risk Assessment of 1,3 Dichloropropene, California Department of Pesticide Regulation, 1997.70 Toxicology and carcinogenesis studies of 1,3-butadiene (CAS No. 106-99-0) in B6C3F1 mice(inhalation studies), National Toxicology Program (NTP), US Public Health Service, USDepartment of Health and Human Services. (1984) NTP TR 288, NIH Pub. No. 84-2544.Research Triangle Park, NC.71 T. Clary, Tim and Ritz, B. Pancreatic Cancer Mortality and Organochlorine Pesticide Exposurein California 1989-1996, Amer J Indust Med 43:306-313. 2003.72 Metam Sodium Risk Characterization Document, Medical Toxicology Branch, CaliforniaDepartment of Pesticide Regulation, July 21, 2004.73 Evaluation of Methyl Isothiocyanate as a Toxic Air Contaminant, California Department ofPesticide Regulation, August 2002, http://www.cdpr.ca.gov/docs/empm/pubs/tac/finlmenu.htm.74 M.J. Russell, T.I. Rush (Metam Sodium Task Force), Methyl Isothiocyanate: Determination ofHuman Olfactory Threshold and Human No Observable Effect Level for Eye Irritation, ReportNo. RR 96-049B, DPR Vol. 50150-142#149369, 1996.75 M.F. Nesterova (Kiev Research Institute of the Hygiene and Toxicology of Pesticides,Polymers, and Plastics), Standards for Carbathion in Working Zone Air, Hygiene and Sanitation,1969, 34:191-196.76 Evaluation of the Health Risks Associated with the Metam Spill in the Upper Sacramento River,Office of Environmental Health Hazard Assessment, 1992.77 S.M. Brooks, M.A. Weiss, I.L. Bernstein, Reactive airways dysfunction syndrome (RADS):Persistent asthma syndrome after high level irritant exposures, Chest, 1985, 88:376-384.78 M.J. DiBartolomeis, G.V. Alexeeff, A.M. Fan et al., Regulatory approach to assessing healthrisks of toxic chemical releases following transportation accidents, J. Hazardous Materials, 1994,39(2):193-210.79 G.V. Alexeeff, D.J. Shusterman, R.A. Howd, et al., Dose-response assessment of airbornemethyl isothiocyanate (MITC) following a metam sodium spill, Risk Analysis, 1994, 14:191-198.80 US EPA Revised Metam Sodium Exposure Assessment Docket 159-0106, August 2004.81 Op. cit (73).


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82 E. Tegtmeir, M. Duffy, External Costs of Agricultural Production in the United States,International Journal of Agricultural Sustainability,Vol.2, No.1, 1-20, 200483 D. Pimentel, H. Acquay, M. Biltonen, P. Rice, M. Silva, J. Nelson, V. Lipner, S. Giordano, A.Horowitz & M. D’Arnor (1992) Environmental and economic costs of pesticide use. Bioscience.42 (10), 750-760.84 C. Beecher, New book extols Washington State's commitment to sustainability. Capital PressWEST edition, August 26, 2005, p 3.85 A. A. Abdul-Baki, Cover Crops For Vegetable Production In Tropical Areas, AmericanVegetable Grower, March 2005.86M. Bolda, L. Torte, K. Klonsky & J. E. Bervejillo, Sample Costs to Produce OrganicStrawberries, University of California Cooperative Extension, 2003.http://news.ucanr.org/storyshow.cfm?story=597&printver=yes.87M. Bolda, Mark, L. Torte, K. Klonsky & R. L. De Moura, Sample Costs to ProduceStrawberries, University of California Cooperative Extension, 2004.88 M. Gene, K. M. Klonsky & R. L. De Moura, Sample Costs to Produce Processing Tomatoes,University of California Cooperative Extension, 2001 (Davis, CA)89 K. Klonsky, L. Torte & D. Chaney. Production Practices and Sample Costs for OrganicProcessing Tomatoes in the Sacramento Valley, University of California Cooperative Extension,1993-1994 (Davis, CA).90 J. Suskiw, Mustard for Pest Control, Not for Your Sandwich, Agricultural Research Magazine,Vol. 52, No. 10: 14-15, http://www.ars.usda.gov/is/AR/archive/oct04/pest1004.htm.91 J. Nunez, M. Davis. Use of Cover Crops to Suppress Soil borne Pests in Potato, CaliforniaPotato Research Advisory Board Research Grant Proposal, Project Year 2004-2005. For moreinformation contact: Joe Nunez, UC Cooperative Extension, Kern County, 1031 Mount VernonAve., Bakersfield, CA 93307.92 Op. cit (84).93 Op. cit (90).94 D. Bryant. Carrot Research Probes Foreign Cultivars. Western Farm Press, April 16, 2005.http://westernfarmpress.com/mag/farming_carrot_research_probes/. For additional informationplease see, P.W. Simon, W.C. Matthews, P.A. Roberts, Evidence for Simply Inherited DominantResistance to Meloidogyne javanicain in Carrot, Theor Appl Genet (2000) 100:735–742; L.S.Boiteux, J.G. Belter, P.A. Roberts, P.W. Simon, RAPD Linkage Map of the Genomic RegionEncompassing the Root-knot Nematode (Meloidogyne javanica) Resistance Locus in Carrot,Theor Appl Genet (2000) 100:439–446; L.S. Boiteux, J.R. Hyman, I.C. Bach, M.E.N. Fonseca,W.C. Matthews P.A. Roberts, P.W. Simon, Employment of flanking codominant STS markers toestimate allelic substitution effects of a nematode resistance locus in carrot, Euphytica 136:37–44, 2004.95 How to Manage Pests, UC Pest Management Guidelines, Carrots Nematodes, UC IPM OnlineStatewide Integrated Pest Management Program,http://www.ipm.ucdavis.edu/PMG/r102200111.html.

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