TOXICOLOGICAL PROFILE FOR
 

METHYL PARATHION
 

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES
 

Public Health Service
 

Agency for Toxic Substances and Disease Registry
 

September 2001 
METHYL PARATHION ii 

DISCLAIMER 

The use of company or product name(s) is for identification only and does not imply endorsement by the 

Agency for Toxic Substances and Disease Registry. 
METHYL PARATHION iii 

UPDATE STATEMENT
 

Toxicological profiles are revised and republished as necessary, but no less than once every three years. 

For information regarding the update status of previously released profiles, contact ATSDR at: 

Agency for Toxic Substances and Disease Registry
 

Division of Toxicology/Toxicology Information Branch
 

1600 Clifton Road NE, E-29
 

Atlanta, Georgia 30333
 


METHYL PARATHION vi 

*Legislative Background 

The toxicological profiles are developed in response to the Superfund Amendments and 

Reauthorization Act (SARA) of 1986 (Public law 99-499) which amended the Comprehensive 

Environmental Response, Compensation, and Liability Act of 1980 (CERCLA or Superfund). This 

public law directed ATSDR to prepared toxicological profiles for hazardous substances most commonly 

found at facilities on the CERCLA National Priorities List and that pose the most significant potential 

threat to human health, as determined by ATSDR and the EPA. The availability of the revised priority 

list of 275 hazardous substances was announced in the Federal Register on November 17, 1997 (62 FR 

61332). For prior versions of the list of substances, see Federal Register notices dated April 29, 1996 (61 

FR 18744); April 17, 1987 (52 FR 12866); October 20, 1988 (53 FR 41280); October 26, 1989 (54 FR 

43619); October 17, 1990 (55 FR 42067); October 17, 1991 (56 FR 52166); October 28, 1992 (57 FR 

48801); and February 28, 1994 (59 FR 9486). Section 104(i)(3) of CERCLA, as amended, directs the 

Administrator of ATSDR to prepare a toxicological profile for each substance on the list. 
 

 

METHYL PARATHION vii 

QUICK REFERENCE FOR HEALTH CARE PROVIDERS 

Toxicological Profiles are a unique compilation of toxicological information on a given hazardous 

substance. Each profile reflects a comprehensive and extensive evaluation, summary, and interpretation of 

available toxicologic and epidemiologic information on a substance. Health care providers treating 

patients potentially exposed to hazardous substances will find the following information helpful for fast 

answers to often-asked questions. 

Primary Chapters/Sections of Interest 

Chapter 1: Public Health Statement: The Public Health Statement can be a useful tool for educating 

patients about possible exposure to a hazardous substance. It explains a substance’s relevant 

toxicologic properties in a nontechnical, question-and-answer format, and it includes a review of 

the general health effects observed following exposure. 

Chapter 2: Relevance to Public Health: The Relevance to Public Health Section evaluates, interprets, and 

assesses the significance of toxicity data to human health. 

Chapter 3: Health Effects: Specific health effects of a given hazardous compound are reported by type of 

health effect (death, systemic, immunologic, reproductive), by route of exposure, and by length of 

exposure (acute, intermediate, and chronic). In addition, both human and animal studies are 

reported in this section. 

NOTE: Not all health effects reported in this section are necessarily observed in 

the clinical setting. Please refer to the Public Health Statement to identify 

general health effects observed following exposure. 

Pediatrics: Four new sections have been added to each Toxicological Profile to address child health 

issues: 

Section 1.6 How Can (Chemical X) Affect Children? 

Section 1.7 How Can Families Reduce the Risk of Exposure to (Chemical X)? 

Section 3.7 Children’s Susceptibility 

Section 6.6 Exposures of Children 

Other Sections of Interest: 

Section 3.8 Biomarkers of Exposure and Effect 

Section 3.11 Methods for Reducing Toxic Effects 

ATSDR Information Center 

Phone: 1-888-42-ATSDR or (404) 639-6357 Fax: (404) 639-6359 

E-mail: atsdric@cdc.gov Internet: http://www.atsdr.cdc.gov 

The following additional material can be ordered through the ATSDR Information Center: 

Case Studies in Environmental Medicine: Taking an Exposure History—The importance of taking an 

exposure history and how to conduct one are described, and an example of a thorough exposure 

history is provided. Other case studies of interest include Reproductive and Developmental 

Hazards; Skin Lesions and Environmental Exposures; Cholinesterase-Inhibiting Pesticide 

Toxicity; and numerous chemical-specific case studies. 
METHYL PARATHION viii 

Managing Hazardous Materials Incidents is a three-volume set of recommendations for on-scene 

(prehospital) and hospital medical management of patients exposed during a hazardous materials incident. 

Volumes I and II are planning guides to assist first responders and hospital emergency department 

personnel in planning for incidents that involve hazardous materials. Volume III—Medical Management 

Guidelines for Acute Chemical Exposures—is a guide for health care professionals treating patients 

exposed to hazardous materials. 

Fact Sheets (ToxFAQs) provide answers to frequently asked questions about toxic substances. 

Other Agencies and Organizations 

The National Center for Environmental Health (NCEH) focuses on preventing or controlling disease, 

injury, and disability related to the interactions between people and their environment outside the 

workplace. Contact: NCEH, Mailstop F-29, 4770 Buford Highway, NE, Atlanta, GA 30341­

3724 • Phone: 770-488-7000 • FAX: 770-488-7015. 

The National Institute for Occupational Safety and Health (NIOSH) conducts research on occupational 

diseases and injuries, responds to requests for assistance by investigating problems of health and 

safety in the workplace, recommends standards to the Occupational Safety and Health 

Administration (OSHA) and the Mine Safety and Health Administration (MSHA), and trains 

professionals in occupational safety and health. Contact: NIOSH, 200 Independence Avenue, 

SW, Washington, DC 20201 • Phone: 800-356-4674 or NIOSH Technical Information Branch, 

Robert A. Taft Laboratory, Mailstop C-19, 4676 Columbia Parkway, Cincinnati, OH 45226-1998 

• Phone: 800-35-NIOSH. 

The National Institute of Environmental Health Sciences (NIEHS) is the principal federal agency for 

biomedical research on the effects of chemical, physical, and biologic environmental agents on 

human health and well-being. Contact: NIEHS, PO Box 12233, 104 T.W. Alexander Drive, 

Research Triangle Park, NC 27709 • Phone: 919-541-3212. 

Referrals 

The Association of Occupational and Environmental Clinics (AOEC) has developed a network of clinics 

in the United States to provide expertise in occupational and environmental issues. Contact: 

AOEC, 1010 Vermont Avenue, NW, #513, Washington, DC 20005 • Phone: 202-347-4976 

• FAX: 202-347-4950 • e-mail: AOEC@AOEC.ORG • Web Page: http://www.aoec.org/. 

The American College of Occupational and Environmental Medicine (ACOEM) is an association of 

physicians and other health care providers specializing in the field of occupational and 

environmental medicine. Contact: ACOEM, 55 West Seegers Road, Arlington Heights, IL 

60005 • Phone: 847-818-1800 • FAX: 847-818-9266. 
METHYL PARATHION ix 

CONTRIBUTORS 

CHEMICAL MANAGER(S)/AUTHORS(S):
 

Jewell D. Wilson, Ph.D.
 

ATSDR, Division of Toxicology, Atlanta, GA
 

Joan Colman, Ph.D.
 

David Wohlers, Ph.D.
 

Syracuse Research Corporation, North Syracuse, NY
 

Cheryl Sutton, Ph.D.
 

Syracuse Research Corporation, Arlington, VA
 

THE PROFILE HAS UNDERGONE THE FOLLOWING ATSDR INTERNAL REVIEWS:
 

1.	 Health Effects Review. The Health Effects Review Committee examines the health effects 

chapter of each profile for consistency and accuracy in interpreting health effects and classifying 

end points. 

2.	 Minimal Risk Level Review. The Minimal Risk Level Workgroup considers issues relevant to 

substance-specific minimal risk levels (MRLs), reviews the health effects database of each 

profile, and makes recommendations for derivation of MRLs. 

3.	 Data Needs Review. The Research Implementation Branch reviews data needs sections to assure 

consistency across profiles and adherence to instructions in the Guidance. 

METHYL PARATHION xi 

PEER REVIEW
 

A peer review panel was assembled for methyl parathion. The panel consisted of the following members: 

1.	 Donald Morgan, M.D./Ph.D., Private Consultant, Cedar Rapids, Iowa; 

2.	 Shane Que Hee, Ph.D., Department of Environmental Health Sciences, UCLA School of Public 

Health, Los Angeles, California; 

3.	 Michael Utidjian, M.D., Private Consultant, Wayne, New Jersey. 

These experts collectively have knowledge of methyl parathion's physical and chemical properties, 

toxicokinetics, key health end points, mechanisms of action, human and animal exposure, and 

quantification of risk to humans. All reviewers were selected in conformity with the conditions for peer 

review specified in Section 104(I)(13) of the Comprehensive Environmental Response, Compensation, 

and Liability Act, as amended. 

Scientists from the Agency for Toxic Substances and Disease Registry (ATSDR) have reviewed the peer 

reviewers' comments and determined which comments will be included in the profile. A listing of the 

peer reviewers' comments not incorporated in the profile, with a brief explanation of the rationale for their 

exclusion, exists as part of the administrative record for this compound. A list of databases reviewed and 

a list of unpublished documents cited are also included in the administrative record. 

The citation of the peer review panel should not be understood to imply its approval of the profile's final 

content. The responsibility for the content of this profile lies with the ATSDR. 

METHYL PARATHION xiii 

CONTENTS
 

FOREWORD ...................................................................... v 
 

QUICK REFERENCE FOR HEALTH CARE PROVIDERS ................................. vii 
 

CONTRIBUTORS ................................................................... ix 
 

PEER REVIEW ..................................................................... xi 
 

LIST OF FIGURES ................................................................ xvii 
 

LIST OF TABLES .................................................................. xix 
 

1. PUBLIC HEALTH STATEMENT .................................................... 1 
 

1.1 	 WHAT IS METHYL PARATHION? ............................................ 1 
 

1.2	 WHAT HAPPENS TO METHYL PARATHION WHEN IT ENTERS THE 

ENVIRONMENT? ........................................................... 2 
 

1.3 	 HOW MIGHT I BE EXPOSED TO METHYL PARATHION? ........................ 2 
 

1.4	 HOW CAN METHYL PARATHION ENTER AND LEAVE MY BODY? ............... 4 
 

1.5	 HOW CAN METHYL PARATHION AFFECT MY HEALTH? ....................... 4 
 

1.6	 HOW CAN METHYL PARATHION AFFECT CHILDREN? ......................... 5 
 

1.7	 HOW CAN FAMILIES REDUCE THE RISK OF EXPOSURE TO METHYL 

PARATHION? .............................................................. 6 
 

1.8	 IS THERE A MEDICAL TEST TO DETERMINE WHETHER I HAVE BEEN EXPOSED TO
 

METHYL PARATHION? ..................................................... 8 
 

1.9	 WHAT RECOMMENDATIONS HAS THE FEDERAL GOVERNMENT MADE TO
 

PROTECT HUMAN HEALTH? ................................................ 9 
 

1.10 WHERE CAN I GET MORE INFORMATION? .................................. 10 
 

2. RELEVANCE TO PUBLIC HEALTH ............................................... 11 
 

2.1	 BACKGROUND AND ENVIRONMENTAL EXPOSURES TO METHYL PARATHION IN
 

THE UNITED STATES ...................................................... 11 
 

2.2	 SUMMARY OF HEALTH EFFECTS ........................................... 13 
 

2.3 	 MINIMAL RISK LEVELS ................................................... 17 
 

3. HEALTH EFFECTS .............................................................. 19 
 

3.1	 INTRODUCTION .......................................................... 19 
 

3.2	 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE ................. 19 
 

3.2.1 Inhalation Exposure .................................................. 21 
 

3.2.1.1 Death ..................................................... 21 
 

3.2.1.2 Systemic Effects ............................................ 24 
 

3.2.1.3 Immunological and Lymphoreticular Effects ...................... 25 
 

3.2.1.4 Neurological Effects ......................................... 25 
 

3.2.1.5 Reproductive Effects ......................................... 27 
 

3.2.1.6 Developmental Effects ....................................... 27 
 

3.2.1.7 Cancer .................................................... 27 
 

3.2.2 Oral Exposure ...................................................... 27 
 

3.2.2.1 Death ..................................................... 27 
 
METHYL PARATHION xiv 

3.2.2.2 Systemic Effects ............................................ 29 
 

3.2.2.3 Immunological and Lymphoreticular Effects ...................... 48 
 

3.2.2.4 Neurological Effects ......................................... 49 
 

3.2.2.5 Reproductive Effects ......................................... 53 
 

3.2.2.6 Developmental Effects ....................................... 53 
 

3.2.2.7 Cancer .................................................... 55 
 

3.2.3 Dermal Exposure .................................................... 56 
 

3.2.3.1 Death ..................................................... 56 
 

3.2.3.2 Systemic Effects ............................................ 58 
 

3.2.3.3 Immunological and Lymphoreticular Effects ...................... 58 
 

3.2.3.4 Neurological Effects ......................................... 58 
 

3.2.3.5 Reproductive Effects ......................................... 59 
 

3.2.3.6 Developmental Effects ....................................... 59 
 

3.2.3.7 Cancer .................................................... 60 
 

3.2.4 Other Routes of Exposure ............................................. 60 
 

3.3 GENOTOXICITY .......................................................... 61 
 

3.4 TOXICOKINETICS ......................................................... 67 
 

3.4.1 Absorption ......................................................... 67 
 

3.4.1.1 Inhalation Exposure .......................................... 67 
 

3.4.1.2 Oral Exposure .............................................. 68 
 

3.4.1.3 Dermal Exposure ............................................ 69 
 

3.4.2 	 Distribution ........................................................ 70 
 

3.4.2.1 Inhalation Exposure .......................................... 70 
 

3.4.2.2 Oral Exposure .............................................. 70 
 

3.4.2.3 Dermal Exposure ............................................ 71 
 

3.4.2.4 Other Routes of Exposure ..................................... 71 
 

3.4.3 	 Metabolism ......................................................... 72 
 

3.4.4 	 Elimination and Excretion ............................................. 75 
 

3.4.4.1 Inhalation Exposure .......................................... 75 
 

3.4.4.2 Oral Exposure .............................................. 75 
 

3.4.4.3 Dermal Exposure ............................................ 76 
 

3.4.4.4 Other Routes of Exposure ..................................... 77 
 

3.4.5	 Physiologically Based Pharmacokinetic (PBPK)/Pharmacodynamic (PD) 

Models ............................................................ 77 
 

3.5 MECHANISMS OF ACTION ................................................. 80 
 

3.5.1 	 Pharmacokinetic Mechanisms .......................................... 80 
 

3.5.2 	 Mechanisms of Toxicity ............................................... 81 
 

3.5.3 	 Animal-to-Human Extrapolations ....................................... 83 
 

3.6 ENDOCRINE DISRUPTION ................................................. 84 
 

3.7 CHILDREN’S SUSCEPTIBILITY ............................................. 87 
 

3.8 BIOMARKERS OF EXPOSURE AND EFFECT .................................. 91 
 

3.8.1 Biomarkers Used to Identify or Quantify Exposure to Methyl Parathion ......... 92 
 

3.8.2 Biomarkers Used to Characterize Effects Caused by Methyl Parathion .......... 93 
 

3.9 INTERACTIONS WITH OTHER CHEMICALS .................................. 95 
 

3.10 POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE ....................... 96 
 

3.11 METHODS FOR REDUCING TOXIC EFFECTS ................................. 97 
 

3.11.1 Reducing Peak Absorption Following Exposure ............................ 98 
 

3.11.2 Reducing Body Burden ............................................... 99 
 

3.11.3 Interfering with the Mechanism of Action for Toxic Effects ................... 99 
 

3.12 ADEQUACY OF THE DATABASE ........................................... 100 
 

3.12.1 Existing Information on Health Effects of Methyl Parathion ................. 100 
 
METHYL PARATHION xv 

3.12.2 Identification of Data Needs .......................................... 102 
 

3.12.3 Ongoing Studies .................................................... 111 
 

4. CHEMICAL AND PHYSICAL INFORMATION ...................................... 113 
 

4.1 CHEMICAL IDENTITY .................................................... 113 
 

4.2 PHYSICAL AND CHEMICAL PROPERTIES ................................... 113 
 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL ............................ 117 
 

5.1 PRODUCTION ........................................................... 117 
 

5.2 IMPORT/EXPORT ........................................................ 119 
 

5.3 USE ..................................................................... 119 
 

5.4 DISPOSAL ............................................................... 123 
 

6. POTENTIAL FOR HUMAN EXPOSURE ........................................... 125 
 

6.1 OVERVIEW .............................................................. 125 
 

6.2 RELEASES TO THE ENVIRONMENT ........................................ 127 
 

6.2.1 Air .............................................................. 127 
 

6.2.2 Water ............................................................ 128 
 

6.2.3 Soil .............................................................. 130 
 

6.3 ENVIRONMENTAL FATE .................................................. 130 
 

6.3.1 Transport and Partitioning ............................................ 131 
 

6.3.2 Transformation and Degradation ....................................... 133 
 

6.3.2.1 Air ...................................................... 133 
 

6.3.2.2 Water .................................................... 133 
 

6.3.2.3 Sediment and Soil .......................................... 135 
 

6.3.2.4 Environmental Media ....................................... 136 
 

6.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT ............... 136 
 

6.4.1 Air .............................................................. 136 
 

6.4.2 Water ............................................................ 138 
 

6.4.3 Sediment and Soil .................................................. 139 
 

6.4.4 Other Environmental Media ........................................... 140 
 

6.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE .................. 142 
 

6.6 EXPOSURES OF CHILDREN ............................................... 144 
 

6.7 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES ...................... 146 
 

6.8 ADEQUACY OF THE DATABASE ........................................... 147 
 

6.8.1 Identification of Data Needs .......................................... 148 
 

6.8.2 Ongoing Studies .................................................... 151 
 

7. ANALYTICAL METHODS ....................................................... 155 
 

7.1 BIOLOGICAL SAMPLES ................................................... 155 
 

7.2 ENVIRONMENTAL SAMPLES .............................................. 158 
 

7.3 ADEQUACY OF THE DATABASE ........................................... 162 
 

7.3.1 Identification of Data Needs .......................................... 163 
 

7.3.2 Ongoing Studies .................................................... 164 
 

8. REGULATIONS AND ADVISORIES .............................................. 165 
 

9. REFERENCES ................................................................. 171 
 

10. GLOSSARY .................................................................. 221 
 
METHYL PARATHION xvi 

APPENDICES 

A. ATSDR MINIMAL RISK LEVELS AND WORKSHEETS ......................... A-1 
 

B. USER’S GUIDE ........................................................... B-1 
 

C. ACRONYMS, ABBREVIATIONS, AND SYMBOLS ............................. C-1 
 

D. INDEX .................................................................. D-1 
 
METHYL PARATHION xvii 

LIST OF FIGURES 

3-1. Levels of Significant Exposure to Methyl Parathion - Inhalation ......................... 23 
 

3-2. Levels of Significant Exposure to Methyl Parathion - Oral .............................. 40 
 

3-3. Proposed Metabolic Pathways of Methyl Parathion .................................... 73 
 

3-4. Conceptual Representation of a Physiologically Based Pharmacokinetic (PBPK) Model for a 

Hypothetical Chemical Substance ................................................. 79 
 

3-5. Existing Information on Health Effects of Methyl Parathion ............................ 101 
 

6-1. Frequency of NPL Sites with Methyl Parathion Contamination .......................... 126 
 

METHYL PARATHION xix 

LIST OF TABLES 

3-1. Levels of Significant Exposure to Methyl Parathion - Inhalation ......................... 22 
 

3-2. Plasma and Erythrocyte Cholinesterase Levels in Children Intoxicated by Methyl Parathion .... 26 
 

3-3. Levels of Significant Exposure to Methyl Parathion - Oral .............................. 30 
 

3-4. Levels of Significant Exposure to Methyl Parathion - Dermal ............................ 57 
 

3-5. Genotoxicity of Methyl Parathion In Vivo ............................................ 63 
 

3-6. Genotoxicity of Methyl Parathion In Vitro ........................................... 64 
 

4-1. Chemical Identity of Methyl Parathion ............................................. 114 
 

5-1. Facilities that Produce, Process, or Use Methyl Parathion .............................. 118 
 

5-2. Methyl Parathion Use in Crop Production in 1992 .................................... 121 
 

6-1. Releases to the Environment from Facilities that Produce, Process, or Use Methyl Parathion . . . 129
 

6-2. Ongoing Studies of Methyl Parathion Found in Federal Research in Progress ............... 152 
 

7-1. Analytical Methods for Determining Methyl Parathion and Metabolites in 

Biological Materials ........................................................... 156 
 

7-2. Analytical Methods for Determining Methyl Parathion in Environmental Samples ........... 159 
 

8-1. Regulations and Guidelines Applicable to Methyl Parathion ............................ 166 
 

METHYL PARATHION 1 

1. PUBLIC HEALTH STATEMENT
 

This public health statement tells you about methyl parathion and the effects of exposure. 

The Environmental Protection Agency (EPA) identifies the most serious hazardous waste sites in 

the nation. These sites make up the National Priorities List (NPL) and are the sites targeted for 

long-term federal cleanup activities. Methyl parathion has been found in at least 16 of the 

1,585 current or former NPL sites. However, the total number of NPL sites evaluated for this 

substance is not known. As more sites are evaluated, the sites at which methyl parathion is 

found may increase. This information is important because exposure to this substance may harm 

you and because these sites may be sources of exposure. 

When a substance is released from a large area, such as an industrial plant, or from a container, 

such as a drum or bottle, it enters the environment. This release does not always lead to 

exposure. You are exposed to a substance only when you come in contact with it. You may be 

exposed by breathing, eating, or drinking the substance, or by skin contact. 

If you are exposed to methyl parathion, many factors determine whether you’ll be harmed. 

These factors include the dose (how much), the duration (how long), and how you come in 

contact with it. You must also consider the other chemicals you’re exposed to and your age, sex, 

diet, family traits, lifestyle, and state of health. 

1.1 WHAT IS METHYL PARATHION? 

Methyl parathion is a pesticide that is used to kill insects on crops. Usually, it is sprayed on the 

crops. Methyl parathion comes in two forms: a pure form of white crystals and a technical-grade 

solution (brownish liquid), which contains methyl parathion (80%) and inactive ingredients in a 

solvent. The technical-grade methyl parathion smells like rotten eggs or garlic. Methyl 

parathion is a manufactured chemical, so it is found in the environment only as a result of its 

manufacture or use. Methyl parathion has been manufactured in the United States since 1952 

and has been used to kill insects on many types of crops since this time. Because methyl 
METHYL PARATHION 2 

1. PUBLIC HEALTH STATEMENT 

parathion can be dangerous to humans, the EPA has restricted how it can be used and applied. 

Methyl parathion must be sprayed on crops from the air or from the ground in certain ways to 

minimize the danger of being exposed, and only trained people are allowed to spray methyl 

parathion. Methyl parathion is no longer used on food crops commonly consumed by children, 

and the maximum amount of methyl parathion that can be present as a residue on specific crops 

is regulated (see Section 1.9). In these ways, exposure to methyl parathion can be controlled and 

accidental exposures can be prevented. 

1.2	 WHAT HAPPENS TO METHYL PARATHION WHEN IT ENTERS THE 

ENVIRONMENT? 

Once methyl parathion is introduced into the environment from spraying on crops, droplets of 

methyl parathion in the air fall on soil, plants, or water. While most of the methyl parathion will 

stay in the areas where it is applied, some can move to areas away from where it was applied by 

rain, fog, and wind. Methyl parathion stays in the environment from a few days to several 

months. It is degraded to other chemical compounds by water, sunlight, and bacteria found in 

soil and water. On soil, methyl parathion sticks to the soil, and then is rapidly degraded by 

bacteria. It generally does not leach through the ground and end up in the groundwater. In 

water, methyl parathion breaks down quickly by the action of the water, bacteria in the water, 

and sunlight. In water and air, methyl parathion is broken down by sunlight to form a more toxic 

product called methyl paraoxon. If concentrated amounts of methyl parathion are present in soil, 

such as at landfills and hazardous waste sites, methyl parathion does not degrade as fast. For 

more information, see Chapters 4, 5, and 6. 

1.3	 HOW MIGHT I BE EXPOSED TO METHYL PARATHION? 

Most people are not exposed to methyl parathion in the air they breathe or on things they touch, 

unless they live next to areas being sprayed. The people who are at the greatest risk of being 

exposed to methyl parathion are those who work with this chemical. These include farm 

workers, chemical sprayers, and people who work in factories that make methyl parathion. They 

are exposed to methyl parathion on things they touch where it can pass through their skin, or by 
METHYL PARATHION 3 

1. PUBLIC HEALTH STATEMENT 

breathing it after it has been sprayed. Overexposure to methyl parathion may cause severe 

poisoning or death. Persons may be exposed to dangerous amounts if they go into fields too 

soon after spraying. The people most likely to be exposed to methyl parathion can be protected 

by wearing special clothing and breathing equipment and by staying out of sprayed fields for at 

least 2 days. 

Individuals can also be exposed if they live near landfills where methyl parathion has been 

dumped or near water containing methyl parathion that washes off nearby land or that is 

accidentally spilled. The greatest amounts of methyl parathion are expected to be present near or 

on the farms where methyl parathion is used. After spraying, some methyl parathion can be 

transported by the wind or fog to areas away from where it is used, but the amounts present at 

these locations are not expected to be at dangerous levels. In 1988, one location in Mississippi 

had groundwater that contained 88 parts of methyl parathion per billion parts of water (ppb). 

More recent studies of water samples taken near where methyl parathion was sprayed indicate 

methyl parathion is not found in the groundwater. The risk of exposure to methyl parathion from 

drinking groundwater appears to be low, but the EPA is currently examining this issue. For 

more information, see Chapter 6. 

Methyl parathion is approved only for use on crops. The maximum amount of methyl parathion 

residue allowed by the Food and Drug Administration (FDA) and EPA on crops used as food is 

0.1–1 ppm. The FDA has monitored the food supply for pesticides for a number of years. FDA 

purchases many kinds of foods through Market Basket Surveys and analyzes them for residue 

levels of pesticides. These FDA studies allow scientists to estimate the daily intake of 

pesticides. Generally, the FDA monitoring studies conclude that the U.S. food supply contains 

only very small amounts of pesticides that are not a concern. However, there have been some 

reports of the illegal use of methyl parathion inside homes. For more information, see 

Section 1.7 and Chapter 6. 
METHYL PARATHION 4 

1. PUBLIC HEALTH STATEMENT 

1.4 HOW CAN METHYL PARATHION ENTER AND LEAVE MY BODY? 

Methyl parathion can enter your body if you eat food or drink water containing it; if you swim, 

bathe, or shower in contaminated water; if you touch recently sprayed plants or soil; if you touch 

contaminated soil near hazardous waste sites; or if you breathe air that contains methyl 

parathion, such as near factories or recently sprayed farm fields (or in recent accounts of the 

illegal use of methyl parathion, if you breathe air or touch contaminated surfaces inside homes 

where methyl parathion has been used to kill insects). By any means of exposure, methyl 

parathion goes into your body quickly and gets into your blood. From your bloodstream, methyl 

parathion goes to your liver, brain, and other organs. Your liver changes some of methyl 

parathion to a more harmful chemical called methyl paraoxon. Both methyl parathion and 

methyl paraoxon can bind to enzymes of your nerves within minutes or hours. Your liver breaks 

down methyl parathion and methyl paraoxon into less harmful substances. These less harmful 

substances leave your body in urine within hours or days. For more information, see Chapter 3. 

1.5 HOW CAN METHYL PARATHION AFFECT MY HEALTH? 

Methyl parathion interferes with the normal way that the nerves and brain function. Exposure to 

very high levels of methyl parathion for a short period in air or water may cause death, loss of 

consciousness, dizziness, confusion, headaches, difficult breathing, chest tightness, wheezing, 

vomiting, diarrhea, cramps, tremors, blurred vision, and sweating. Some people who have been 

exposed to substances similar to methyl parathion have experienced changes in mental state that 

lasted several months after exposure to high levels of these substances ended. If people are 

exposed to levels of methyl parathion below those that affect nerve function, few or no health 

problems seem to occur. There is no evidence that methyl parathion causes birth defects in 

humans or affects the ability of humans to produce children. There is also no proof that methyl 

parathion causes cancer in people who are regularly exposed, such as farmers and pesticide 

applicators. 

To protect the public from the harmful effects of toxic chemicals and to find ways to treat people 

who have been harmed, scientists use many tests. 
METHYL PARATHION 5 

1. PUBLIC HEALTH STATEMENT 

One way to see if a chemical will hurt people is to learn how the chemical is absorbed, used, and 

released by the body; for some chemicals, animal testing may be necessary. Animal testing may 

also be used to identify health effects such as cancer or birth defects. Without laboratory 

animals, scientists would lose a basic method to get information needed to make wise decisions 

to protect public health. Scientists have the responsibility to treat research animals with care and 

compassion. Laws today protect the welfare of research animals, and scientists must comply 

with strict animal care guidelines. 

Animal studies show effects of methyl parathion similar to those seen in people. In addition, 

short-term high exposure of animals to methyl parathion caused decreased heart rate. This may 

be the result of methyl parathion's effects on the nerves that control the heart. Methyl parathion 

decreased the ability of animals to fight infections in some studies, but not in others. It is not 

known whether any of these effects occur in people. It is not known whether methyl parathion 

affects the ability of animals to reproduce. Studies in animals have not shown that methyl 

parathion causes cancer. 

You can find more information on the health effects associated with exposure to methyl 

parathion in Chapters 2 and 3. 

1.6 HOW CAN METHYL PARATHION AFFECT CHILDREN? 

This section discusses potential health effects from exposures during the period from conception 

to maturity at 18 years of age in humans. 

Children are likely to be exposed to methyl parathion in the same ways as adults, mainly by 

eating foods or drinking milk or water that contain residues of this chemical. Because of their 

smaller weight, children’s intake of methyl parathion per kilogram of body weight may be 

greater than that of adults. The FDA and EPA permit residues of pesticides to be present in 

crops used as food, and these amounts are considered to be safe. The EPA, however, has 

recently used stricter regulations and has canceled the use of methyl parathion on food crops 
METHYL PARATHION 6 

1. PUBLIC HEALTH STATEMENT 

commonly eaten by children. As a result, the exposure of children to methyl parathion from 

foods will be very small. 

Children are affected by methyl parathion in the same manner as adults. Exposure to high levels 

of methyl parathion, even for short periods, may result in changes in the nervous system, leading 

to headaches, dizziness, confusion, blurred vision, difficulty breathing, vomiting, diarrhea, loss 

of consciousness, and death (see also Section 1.5 for a more complete description of how methyl 

parathion affects human health). It is not known whether children are more sensitive to the 

effects of methyl parathion than adults. There is some indication that young rats may be more 

sensitive than adults to nervous system effects. 

There is no evidence in humans that methyl parathion causes birth defects. Birth defects have 

not been seen when methyl parathion was given to animals by mouth, but minor birth defects did 

occur in one study in which high doses were injected into pregnant animals. It is not known 

whether these effects occur in people. It is unlikely that people would be exposed by breathing, 

touching, or eating as much methyl parathion as was injected in the animal studies. 

Animal studies have also shown that methyl parathion can be transferred from a pregnant mother 

to the developing fetus. Methyl parathion caused changes in the behavior of young animals 

whose mothers were given methyl parathion during pregnancy, and this effect needs to be 

studied more. Methyl parathion has been detected in small amounts in breast milk, but only in a 

few localities in central Asia. Studies of mother animals fed methyl parathion show that methyl 

parathion can be transferred into their milk and their nursing newborn babies. 

1.7	 HOW CAN FAMILIES REDUCE THE RISK OF EXPOSURE TO METHYL 

PARATHION? 

If your doctor finds that you have been exposed to significant amounts of methyl parathion, ask 

whether your children might also be exposed. Your doctor might need to ask your state health 

department to investigate. 
METHYL PARATHION 7 

1. PUBLIC HEALTH STATEMENT 

The only approved use of methyl parathion is on crops, including crops used as foods. Effective 

December 31, 1999, the EPA cancelled the use of methyl parathion on many kinds of crops used 

as foods because of a concern for exposure risks to children and to workers. This action will 

reduce the risks to families of methyl parathion exposure from food. 

The general population is not likely to be exposed to large amounts of methyl parathion. The 

populations living in the areas where methyl parathion is used on crops, however, may be 

exposed to greater amounts of methyl parathion. Methyl parathion is often detected in foods and 

air samples collected where methyl parathion is used. People who live close to areas of methyl 

parathion use also may be exposed to larger amounts of methyl parathion, because small 

amounts of the pesticide will move from the place where it is used to nearby areas. These 

exposures may include such things as touching contaminated plants, breathing the mist formed 

from the sprayed chemical, drinking contaminated water, or eating recently sprayed fruits and 

vegetables. People who are most likely to receive the highest exposures are those who work in 

the factories that make methyl parathion, workers who spray it on crops, and farmers. Entry of 

methyl parathion into the body after contact with the skin is expected to be the major exposure 

pathway for those working in these operations. Breathing the mist containing methyl parathion 

may also occur. 

Families can reduce the risk of exposure to methyl parathion in the soil, on plants, or in the air 

by staying away from fields that have been recently sprayed. If families wait at least 4–5 days 

before entering sprayed fields, then the amount of methyl parathion present in the air or on plants 

is expected to be small. 

Families should also be aware that sometimes methyl parathion has been illegally sprayed inside 

the home to kill insects. Your children may be exposed to methyl parathion if an unqualified 

person applies pesticides containing it around your home. In some cases, the improper use of 

pesticides banned for use in homes has turned homes into hazardous waste sites. Make sure that 

any person you hire is licensed and, if appropriate, certified to apply pesticides. Your state 

licenses each person who is qualified to apply pesticides according to EPA standards and further 

certifies each person who is qualified to apply “restricted use” pesticides. Ask to see the license 
METHYL PARATHION 8 

1. PUBLIC HEALTH STATEMENT 

and certification. Also ask for the brand name of the pesticide, a Material Safety Data Sheet 

(MSDS), the name of the product’s active ingredient, and the EPA registration number. Ask 

whether EPA has designated the pesticide “for restricted use” and what the approved uses are. 

This information is important if you or your family react to the product. If you buy over-thecounter pesticides products to apply yourself, be sure the products are in unopened pesticide 

containers that are labeled and contain an EPA registration number. Carefully follow the 

instructions on the label. If you plan to spray inside, make sure the products are in unopened 

pesticide containers that are labeled and contain an EPA registration number. Carefully follow 

the instructions on the label. If you plan to spray inside, make sure the pesticide is intended for 

indoor use. If you feel sick after a pesticide has been used in your home, consult your doctor or 

local poison control center. 

1.8	 IS THERE A MEDICAL TEST TO DETERMINE WHETHER I HAVE BEEN 

EXPOSED TO METHYL PARATHION? 

Several medical tests can determine whether you have been exposed to methyl parathion. The 

first medical test measures methyl parathion in your blood or measures 4-nitrophenol, which is a 

breakdown product of methyl parathion, in your urine. These tests are only reliable for about 

24 hours after you are exposed because methyl parathion breaks down quickly and leaves your 

body. These tests cannot tell whether you will have harmful health effects or what those effects 

may be. The next medical test measures the levels of a substance called cholinesterase in your 

blood. If cholinesterase levels are less than half of what they should be and you have been 

exposed to methyl parathion, then you may get symptoms of poisoning. However, lower 

cholinesterase levels may also only indicate exposure and not necessarily harmful effects. The 

action of methyl parathion may cause lower cholinesterase levels in your red blood cells or your 

blood plasma. Such lowering, however, can also be caused by factors other than methyl 

parathion. For example, cholinesterase values may already be low in some people, because of 

heredity or disease. However, a lowering of cholinesterase levels can often show whether 

methyl parathion or similar compounds have acted on your nerves. Cholinesterase levels in red 

blood cells can stay low for more than a month after you have been exposed to methyl parathion 

or similar chemicals. For more information, see Chapters 3 and 7. 
METHYL PARATHION 9 

1. PUBLIC HEALTH STATEMENT 

1.9	 WHAT RECOMMENDATIONS HAS THE FEDERAL GOVERNMENT MADE TO 

PROTECT HUMAN HEALTH? 

The federal government develops regulations and recommendations to protect public health. 

Regulations can be enforced by law. Federal agencies that develop regulations for toxic 

substances include the Environmental Protection Agency (EPA), the Occupational Safety and 

Health Administration (OSHA), and the Food and Drug Administration (FDA). 

Recommendations provide valuable guidelines to protect public health but cannot be enforced by 

law. Federal organizations that develop recommendations for toxic substances include the 

Agency for Toxic Substances and Disease Registry (ATSDR) and the National Institute for 

Occupational Safety and Health (NIOSH). 

Regulations and recommendations can be expressed in not-to-exceed levels in air, water, soil, or 

food that are usually based on levels that affect animals; then they are adjusted to help protect 

people. Sometimes these not-to-exceed levels differ among federal organizations because of 

different exposure times (an 8-hour workday or a 24-hour day), the use of different animal 

studies, or other factors. 

Recommendations and regulations are also periodically updated as more information becomes 

available. For the most current information, check with the federal agency or organization that 

provides it. Some regulations and recommendations for methyl parathion include the following: 

NIOSH recommends that a person not be exposed in the workplace to more than 0.2 mg/m3

 of 

methyl parathion for a 10-hour workday, 40-hour workweek. 

According to EPA, the following levels of methyl parathion in drinking water are not expected to 

cause effects that are harmful to health: 0.3 mg/L for 1 or 10 days of exposure for children, 

0.03 mg/L for longer term exposure for children, and 0.002 mg/L for lifetime exposure of adults. 

It is illegal to use methyl parathion indoors. Methyl parathion is approved only for use on 

agricultural crops. In 1999, EPA canceled the use of methyl parathion on many food crops, 
METHYL PARATHION 10 

1. PUBLIC HEALTH STATEMENT 

particularly those consumed by children, such as apples, peaches, pears, carrots, and peas, and 

also canceled nonfood uses such as ornamental plants and nursery stock uses. Methyl parathion 

use is still allowed on other crops eaten by people or by farm animals. A maximum of 

0.1–1 ppm of methyl parathion is allowed in or on the other crops (fruits, vegetables, nuts, and 

grains) that may be eaten by people. For more information, see Chapter 8. 

1.10 WHERE CAN I GET MORE INFORMATION? 

If you have any more questions or concerns, please contact your community or state health or 

environmental quality department or 

Agency for Toxic Substances and Disease Registry
 

Division of Toxicology
 

1600 Clifton Road NE, Mailstop E-29
 

Atlanta, GA 30333
 

* Information line and technical assistance 

Phone: 1-888-42-ATSDR (1-888-422-8737)
 

Fax: 1-404-498-0057
 

ATSDR can also tell you the location of occupational and environmental health clinics. These 

clinics specialize in recognizing, evaluating, and treating illnesses resulting from exposure to 

hazardous substances. 

* To order toxicological profiles, contact 

National Technical Information Service
 

5285 Port Royal Road
 

Springfield, VA 22161
 

Phone: (800) 553-6847 or (703) 605-6000
 
METHYL PARATHION 11 

2. RELEVANCE TO PUBLIC HEALTH
 

2.1	 BACKGROUND AND ENVIRONMENTAL EXPOSURES TO METHYL PARATHION IN 

THE UNITED STATES 

Methyl parathion is a broad-spectrum agricultural insecticide that is released to the environment primarily 

through spraying of the insecticide on a variety of agricultural products. Once methyl parathion is 

introduced to the environment, it is degraded by hydrolysis, photolysis, or by biodegradation from 

microorganisms found in most sediment, soils, and water. Methyl parathion is primarily confined to the 

application area, but some can be transported by rain, fog, and wind to other areas. Methyl parathion 

adsorbs to the soil and is relatively immobile. As a result, leaching into groundwater is not usually 

observed. Volatilization has been observed to occur from plants and soil post-application, with 

volatilization from plants being the faster of the two. Limited studies show that bioconcentration of 

methyl parathion does not occur to a significant extent; that which is accumulated in plants and animals is 

rapidly metabolized. Methyl parathion is not widely dispersed or persistent in the environment. Residue 

amounts of methyl parathion have been detected in air, water, fish, soil, and agricultural crops consumed 

as foods. 

Methyl parathion is approved by the EPA only for use on agricultural crops. As a result, the general 

population is not likely to be exposed to large amounts of methyl parathion. Some exposure to residues 

of methyl parathion is possible, however, as many studies show that methyl parathion has been detected 

in foods and atmosphere samples. Populations living within or very near areas of heavy methyl parathion 

use would have an increased risk of exposure to large amounts of methyl parathion through dermal 

contact with contaminated plants, by inhalation of the mist formed from the applied insecticide, or by 

ingestion of water or food-borne residues. Those likely to receive the highest levels of exposure are those 

who are involved in the production, formulation, handling, and application of methyl parathion. Dermal 

contact appears to be the major route of exposure, while inhalation may also be an important route of 

exposure for those working in these operations. 

The greatest potential for exposure of the general population to methyl parathion is by consumption of 

food containing residues from spray applications of the insecticide. In a 10-year study, methyl parathion 

was found at an average concentration of 0.0035 ppm in a few examples of ready-to-eat foods. 

Concentrations in the range of 0.05–2.0 ppm were reported in 0.5% of the samples of domestic and 
METHYL PARATHION 12 

2. RELEVANCE TO PUBLIC HEALTH 

imported foods and animal feeds in a 5-year analysis. Additional studies have reported concentrations of 

methyl parathion of 0.016–3.8 ppm in a small percentage of samples of various foods. 

Residues in many foods should decrease because EPA has canceled many of the food crop uses of methyl 

parathion, including fruits and vegetables commonly eaten by children, some other vegetable uses, some 

feed uses, and all nonfood uses such as ornamental plants and nursery stock uses. Tolerances for methyl 

parathion on these foods and feed also have been canceled. This action was taken because of a concern 

for risks to children and workers. Some food and feed uses and tolerances are to be maintained. 

In areas of agricultural methyl parathion usage, both outdoor and indoor air levels of methyl parathion of 

approximately 12 ng/m3

 have been measured, and household dust was found to contain 21 ppb of methyl 

parathion. Outdoor and indoor air concentrations of methyl parathion as high as 0.71 and 9.4 μg/m3

, 

respectively, have been measured at the homes of individuals employed as pesticide formulators. 

Dermal exposure to methyl parathion is not likely to be a health concern to the general population, with 

the possible exception of individuals in the immediate vicinity of a field during application of the 

pesticide. Dermal exposure, however, is a major source of exposure for workers directly involved in the 

manufacture, application, and cleanup of the chemical, and for field workers. Laundry workers cleaning 

the clothing of such workers may also be exposed. 

Children are expected to be exposed to methyl parathion by the same routes that affect adults. Small 

children are more likely to come into contact with methyl parathion residues that may be present in soil 

and dust both outside and inside the home, due to increased hand-to-mouth activity and playing habits. 

Methyl parathion has been detected in a few samples of breast milk, indicating potential for exposure of 

nursing infants. However, available data are not adequate for determination of the importance of this 

route of child exposure. 

Populations residing near hazardous waste disposal sites may be subject to higher levels of methyl 

parathion in environmental media (i.e., air, groundwater, soil) than those experienced by the general 

population. Methyl parathion has been identified in at least 16 of the 1,585 hazardous waste sites that 

have been proposed for inclusion on the EPA National Priorities List (NPL). However, the number of 

sites evaluated for methyl parathion is not known. As more sites are evaluated, the number of sites where 

methyl parathion has been detected may increase. 
 

METHYL PARATHION 13 

2. RELEVANCE TO PUBLIC HEALTH 

See Chapter 6 for more detailed information regarding concentrations of methyl parathion in 

environmental media. 

2.2 SUMMARY OF HEALTH EFFECTS 

Methyl parathion is a highly toxic pesticide, and humans are susceptible to its acute toxic effects by 

various routes of exposure. Signs and symptoms of acute toxicity are typical of those induced by 

organophosphate insecticides as a group. Almost all systemic effects of methyl parathion are related to 

the action of this compound on the nervous system or are secondary to this primary action. Methyl 

parathion and its active metabolite, methyl paraoxon, exert their profound toxic effect by inhibiting the 

activity of acetylcholinesterase in the nervous system and at the motor end-plate. Hydrolysis of 

acetylcholine is inhibited and the neurotransmitter accumulates at its site of action, producing overstimulation of cholinergic end organs. Information regarding effects in humans is limited to a few case 

reports of people acutely exposed to high levels of methyl parathion either by intentional ingestion or by 

multiple-route exposure from direct contact with spray material either in field applications or through 

illegal indoor spraying. Manifestations of acute poisoning are similar in humans and animals and include 

reduced cholinesterase levels in brain, erythrocytes, and plasma, clinical signs of neurological effects such 

as tremors and convulsions, and cardiac arrhythmia. Except for neuropsychiatric disorders reported in 

humans after chronic occupational exposure to organophosphates including methyl parathion, no chronic 

effects have been documented in humans. Effects in animals chronically exposed to methyl parathion 

include hematological and ocular changes. Available data regarding the genotoxicity of methyl parathion 

is inconclusive. Based on the lack of a carcinogenic effect in animals and the lack of evidence to indicate 

a strong genotoxic effect, methyl parathion does not appear to present a substantial carcinogenic risk to 

humans. 

Neurological Effects. Clinical symptoms and signs of methyl parathion intoxication are typical of 

organophosphate poisoning. In mild or moderate cases, patients are alert and oriented; in severe cases, 

they can be confused and ataxic, with slurred speech. Headache, dizziness, and incoordination are 

common. Respiratory symptoms consist of chest tightness, a productive cough, and wheezing. 

Gastrointestinal symptoms are nausea, vomiting, diarrhea, and abdominal cramps. Findings considered 

characteristic of organophosphate intoxication are muscle fasciculations and miosis, although the latter 

sign is not always present. Severely intoxicated patients have extreme salivation, involuntary urination 

and defecation, sweating, lacrimation, bradycardia, and hypotension. Unconsciousness, respiratory arrest 

(due to depression of the respiratory center and paralysis of respiratory muscles), and death can result, the 
METHYL PARATHION 14 

2. RELEVANCE TO PUBLIC HEALTH 

latter from a combination of respiratory and cardiovascular failure. Marked depressions in erythrocyte 

and/or plasma cholinesterase levels are typically observed in individuals exhibiting clinical signs of 

organophosphate poisoning. Available data suggest that a rapid decline in cholinesterase levels may be 

more important than the degree of decline. Neurological signs and depressed cholinesterase levels have 

been observed in animals either acutely exposed to atmospheres containing 264 mg/m3

 of methyl 

parathion or administered single oral doses in the range of 4–8 mg/kg. Rats given single oral doses as 

low as 1.5 mg/kg exhibited significantly depressed plasma, erythrocyte, and brain cholinesterase within 

30 minutes of dosing. 

More subtle psychological symptoms have been reported after acute mild organophosphate intoxication. 

Psychological changes associated with dermal application of a potent organophosphate anticholinesterase 

(an unspecified military chemical) occurred in male volunteers who had no other clinical signs or 

symptoms of toxicity except nausea and vomiting. Psychological changes tended to occur when 

cholinesterase levels were depressed to 10–40% of controls. Changes were a state of altered awareness 

characterized by slowed intellectual and motor processes and difficulty in sustaining attention. Subjects 

felt slowed down, agitated, and confused. These changes may be a concern with exposure to other 

organophosphate insecticides, including methyl parathion. 

Another condition that has been reported as a consequence of very high acute exposures to organophosphate insecticides is the intermediate syndrome. The onset occurs approximately 1–4 days after the 

acute cholinergic crisis has resolved. Clinical observations include acute respiratory insufficiency and 

muscular weakness, primarily of the neck flexors, proximal limb, and respiratory muscles, and motor 

cranial nerve palsies. Death may ensue from respiratory insufficiency. The syndrome is thought to result 

from prolonged acetylcholinesterase inhibition at the neuromuscular junction. The intermediate 

syndrome has been observed primarily in cases of exposure to fenthion, dimethoate, monocrotophos, and 

methamidophos, but also in one case of parathion ingestion, and in a few cases of ingestion and one of 

inhalation of a mixture of parathion and methyl parathion. 

Mental disturbances have been reported after organophosphate exposure. Neuropsychiatric symptoms 

occurred in two aerial applicators, one of whom used methyl parathion as well as other insecticides. One 

of these pilots had high levels of exposure to a mixture containing methyl parathion, toxaphene, and 

Dipterex® when his clothing became saturated when the tank of his aircraft accidentally overflowed. 

Several months after the accident, the subject complained of anxiety, dizziness, emotional lability, and 

frequent and severe disagreements with family members and associates. Similar observations had been 
 

 

METHYL PARATHION 15 

2. RELEVANCE TO PUBLIC HEALTH 

made among a group of 16 men who had worked with a variety of organophosphates over a number of 

years. Exposure was likely by both dermal and inhalation routes. During exposure, the men had periodic 

episodes of acute organophosphate toxicity: nausea, vomiting, excessive perspiration, muscle weakness, 

confusion, etc. When these men consulted psychiatrists or were admitted to mental hospitals, they had 

depressive or schizophrenic manifestations or major impairment of memory and concentration. These 

findings were attributed to the action of organophosphates on acetylcholinesterase in the central nervous 

system. Follow-up of the cases showed that these effects persisted for 6 months after exposure had 

ceased, but had disappeared by 12 months after exposure. 

In animals, longer duration feeding studies have reported plasma, erythrocyte, and brain cholinesterase 

inhibition in dogs at 3.0 mg/kg/day for 13 weeks and in rats at 2.5 mg/kg/day for 2 years. Cholinergic 

signs were seen in the rats during the first few months. Electrophysiological effects were detected in the 

central nervous systems of male rats exposed to methyl parathion through gavage administration of 

0.22 mg/kg/day to the dams on days 5–15 of gestation and days 2–28 of lactation, followed by direct 

administration of the same dose to the male pups for 8 weeks. 

A serious neurological effect of some organophosphates and triarylphosphates, such as tri-ortho-cresylphosphate, is delayed neurotoxicity. Delayed neurotoxicity has been associated with inhibition of a 

neurotoxic esterase in nerve tissue. Axons in the spinal cord and peripheral nerves are targets for 

compound-induced damage. A classic screening test for such an effect is to administer the suspect 

chemical to atropinized chickens and to observe the animals for signs of leg weakness or paralysis. 

Methyl parathion does not appear to be a delayed neurotoxin, although studies in rats suggested that 

chronic oral exposure to 2.5 mg/kg/day methyl parathion may result in distal axonopathy, and 

intermediate oral exposure to 0.22 mg/kg/day may result in decreased nerve conduction velocity and 

increased refractory period. 

Hematological Effects. No information was found regarding hematological effects in humans 

following exposure to methyl parathion. Repeated oral exposure to methyl parathion resulted in 

decreased mean corpuscular volume in one study and decreased hematocrit and erythrocyte count in 

another study in rats. Chronic ingestion of methyl parathion induced reduction of mean hemoglobin, 

hematocrit, and erythrocyte counts in rats. 

Cardiovascular Effects. A number of cardiovascular lesions, such as acute myocardial degeneration 

and vascular degeneration, congestion, and hemorrhage, have been observed in individuals exposed to 
 

 

METHYL PARATHION 16 

2. RELEVANCE TO PUBLIC HEALTH 

fatal doses of methyl parathion. These effects may be secondary to neurological effects of methyl 

parathion on the central and peripheral nervous system and on heart contractility and vascular smooth 

muscle. Acute oral doses of methyl parathion, administered to rats in single doses $9.5 mg/kg, resulted in 

severe cardiac arrhythmias. Similar results were observed following dermal application of doses 

$34 mg/kg. 

Developmental Effects. Adverse effects of methyl parathion on human fetal development have not 

been reported. Based on studies in animals, such effects appear to be possible if pregnant women were 

exposed during the first trimester to high concentrations of methyl parathion that resulted in significant 

depression of cholinesterase levels, particularly if concomitant signs and symptoms of organophosphate 

intoxication occur. Such an exposure scenario may occur with occupational exposure, exposure in homes 

or offices illegally sprayed with methyl parathion, or accidental exposure to methyl parathion, but is less 

likely as a result of low-level exposure. 

The following studies in animals suggest that adverse effects on human fetal development could occur. 

Methyl parathion has been shown to transfer across the placenta of rats after oral exposure of pregnant 

females. Fetotoxicity and offspring with altered brain enzymes and impaired behavior have been reported 

in rats after oral or parenteral maternal administration of methyl parathion at doses that inhibited 

acetylcholinesterase activity and, in some studies, produced cholinergic signs in the dams. Pregnant 

female mice exposed to 60 mg/kg methyl parathion by the intraperitoneal route had a significant increase 

in fetuses with cleft palate compared to control litters. There was also a dose-related increase in fetal 

deaths. These observations suggest that developmental effects may occur in a susceptible population 

exposed to low doses of methyl parathion during pregnancy. 

In addition, oral administration of methyl parathion at relatively low doses to male rats through the dams 

during gestation and lactation and then directly to the offspring until 12 weeks of age resulted in electrophysiological changes in the brain and peripheral nervous system, as described under neurological effects. 

These effects were seen at dose levels that did not cause cholinergic signs; cholinesterase activity was not 

monitored. Such effects were not seen in the same study when the period of administration was confined 

to gestation and lactation. 

Ocular Effects. Pinpoint pupils (miosis) have been observed in individuals following acute exposure 

to methyl parathion. Electroretinographic changes have been reported in mice following intraperitoneal 

injection of 1.5 mg of methyl parathion. These changes were a direct effect of methyl parathion on 
METHYL PARATHION 17 

2. RELEVANCE TO PUBLIC HEALTH 

repolarization of retinal photoreceptors. Other data from animal studies indicate that oral exposure to 

methyl parathion may induce retinal degeneration and bilateral retinal atrophy. The relevance of the 

ocular effects noted in animals to humans is unknown. 

2.3 MINIMAL RISK LEVELS 

Inhalation MRLs 

Although a number of studies have reported the effects of inhalation exposure to methyl parathion in 

humans, no inhalation MRLs were derived based on human data because of the lack of adequate 

quantitative exposure information. Animal data were also insufficient to support the derivation of an 

acute-, intermediate-, or chronic-duration inhalation MRL. 

Oral MRLs 

No acute oral MRL was derived for methyl parathion because data regarding the most sensitive effect that 

was observed after acute oral exposure are conflicting. Increased pup mortality and altered behavior 

occurred in offspring of rats exposed to 1 mg/kg/day methyl parathion during, but no effects on pup 

survival or on sensitive electrophysiological indices of neurotoxicity were seen at virtually the same dose, 

0.88 mg/kg/day, in a similar developmental toxicity study. 

C An MRL of 0.0007 mg/kg/day has been derived for intermediate-duration oral exposure 

(15–364 days) to methyl parathion. 

An intermediate-duration oral MRL of 0.0007 mg/kg/day was derived for methyl parathion based on the 

observation of electrophysiological effects in the central and peripheral nervous systems of male rats 

exposed to methyl parathion through gavage administration of 0.22 mg/kg/day to the dams on days 5–15 

of gestation and days 2–28 of lactation, followed by direct administration of the same dose to the male 

pups for 8 weeks. More marked effects occurred at the two higher doses, 0.44 and 0.88 mg/kg/day. The 

effects were dose-related, and were statistically significant at all three dose levels. The MRL was derived 

by dividing the LOAEL from this study (0.22 mg/kg/day) by an uncertainty factor of 300 (3 for a minimal 

LOAEL, 10 for extrapolation from animals to humans, and 10 for human variability). 

C An MRL of 0.0003 mg/kg/day has been derived for chronic-duration oral exposure (365 days or 

more) to methyl parathion. 
METHYL PARATHION 18 

2. RELEVANCE TO PUBLIC HEALTH 

A chronic-duration oral MRL of 0.0003 mg/kg/day was derived for methyl parathion based on the 

observation of reduced mean hematocrit and erythrocyte counts in rats fed methyl parathion in the diet for 

2 years. Significantly decreased mean hematocrit and erythrocyte counts were observed at 24 months in 

males that consumed 0.25 and 2.5 mg/kg/day for 24 months; no effect on these end points in males was 

observed at 0.025 mg/kg/day. Significantly decreased mean hemoglobin, hematocrit, and erythrocyte 

counts were seen at 6–24 months in females that ingested 2.5 mg/kg/day, with no effect at 

0.025–0.25 mg/kg/day. In the same study, significantly decreased plasma, erythrocyte, and brain 

cholinesterase activities, and abnormal gait, tremor, and peripheral neuropathy, were observed in the rats 

that consumed 2.5 mg/kg/day methyl parathion, but not in rats consuming the lower doses. The MRL 

was derived by dividing the NOAEL of 0.025 mg/kg/day for hematological effects in this study by an 

uncertainty factor of 100 (10 for extrapolation from animals to humans and 10 for human variability). 
METHYL PARATHION 19 

3. HEALTH EFFECTS 

3.1 INTRODUCTION 

The primary purpose of this chapter is to provide public health officials, physicians, toxicologists, and 

other interested individuals and groups with an overall perspective on the toxicology of methyl parathion. 

It contains descriptions and evaluations of toxicological studies and epidemiological investigations and 

provides conclusions, where possible, on the relevance of toxicity and toxicokinetic data to public health. 

A glossary and list of acronyms, abbreviations, and symbols can be found at the end of this profile. 

3.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE 

To help public health professionals and others address the needs of persons living or working near 

hazardous waste sites, the information in this section is organized first by route of exposure (inhalation, 

oral, and dermal) and then by health effect (death, systemic, immunological, neurological, reproductive, 

developmental, genotoxic, and carcinogenic effects). These data are discussed in terms of three exposure 

periods: acute (14 days or less), intermediate (15–364 days), and chronic (365 days or more). 

Levels of significant exposure for each route and duration are presented in tables and illustrated in 

figures. The points in the figures showing no-observed-adverse-effect levels (NOAELs) or 

lowest-observed-adverse-effect levels (LOAELs) reflect the actual doses (levels of exposure) used in the 

studies. LOAELS have been classified into "less serious" or "serious" effects. "Serious" effects are those 

that evoke failure in a biological system and can lead to morbidity or mortality (e.g., acute respiratory 

distress or death). "Less serious" effects are those that are not expected to cause significant dysfunction 

or death, or those whose significance to the organism is not entirely clear. ATSDR acknowledges that a 

considerable amount of judgment may be required in establishing whether an end point should be 

classified as a NOAEL, "less serious" LOAEL, or "serious" LOAEL, and that in some cases, there will be 

insufficient data to decide whether the effect is indicative of significant dysfunction. However, the 

Agency has established guidelines and policies that are used to classify these end points. ATSDR 

believes that there is sufficient merit in this approach to warrant an attempt at distinguishing between 

"less serious" and "serious" effects. The distinction between "less serious" effects and "serious" effects is 

considered to be important because it helps the users of the profiles to identify levels of exposure at which 

major health effects start to appear. LOAELs or NOAELs should also help in determining whether or not 
METHYL PARATHION 20 

3. HEALTH EFFECTS 

the effects vary with dose and/or duration, and place into perspective the possible significance of these 

effects to human health. 

The significance of the exposure levels shown in the Levels of Significant Exposure (LSE) tables and 

figures may differ depending on the user's perspective. Public health officials and others concerned with 

appropriate actions to take at hazardous waste sites may want information on levels of exposure 

associated with more subtle effects in humans or animals (LOAELs) or exposure levels below which no 

adverse effects (NOAELs) have been observed. Estimates of levels posing minimal risk to humans 

(minimal risk levels or MRLs) may be of interest to health professionals and citizens alike. 

Estimates of exposure levels posing minimal risk to humans (Minimal Risk Levels or MRLs) have been 

made for methyl parathion. An MRL is defined as an estimate of daily human exposure to a substance 

that is likely to be without an appreciable risk of adverse effects (noncarcinogenic) over a specified 

duration of exposure. MRLs are derived when reliable and sufficient data exist to identify the target 

organ(s) of effect or the most sensitive health effect(s) for a specific duration within a given route of 

exposure. MRLs are based on noncancerous health effects only and do not consider carcinogenic effects. 

MRLs can be derived for acute, intermediate, and chronic duration exposures for inhalation and oral 

routes. Appropriate methodology does not exist to develop MRLs for dermal exposure. 

Although methods have been established to derive these levels (Barnes and Dourson 1988; EPA 1990c), 

uncertainties are associated with these techniques. Furthermore, ATSDR acknowledges additional 

uncertainties inherent in the application of the procedures to derive less than lifetime MRLs. As an 

example, acute inhalation MRLs may not be protective for health effects that are delayed in development 

or are acquired following repeated acute insults, such as hypersensitivity reactions, asthma, or chronic 

bronchitis. As these kinds of health effects data become available and methods to assess levels of 

significant human exposure improve, these MRLs will be revised. 

A User's Guide has been provided at the end of this profile (see Appendix B). This guide should aid in 

the interpretation of the tables and figures for Levels of Significant Exposure and the MRLs. 
METHYL PARATHION 21 

3. HEALTH EFFECTS 

3.2.1 Inhalation Exposure 

3.2.1.1 Death 

Deaths following exposure to methyl parathion occurred in children (two sisters, aged 4 and 11 years). 

Exposure was by multiple routes including inhalation of methyl parathion that was sprayed inside a house 

from a solution containing 4% methyl parathion (1.25% methyl parathion was recommended by a 

manufacturer for field spraying). Thirteen days after spraying, the house air contained 0.041 mg/m3

, 

7 times the concentration of methyl parathion found just outside. Drinking water, stored in open 

containers due to the lack of running water in the house, contained 0.138–0.275 mg/L of methyl parathion 

12 days after spraying. Dermal exposure may also have been possible. All children in the household, 

including five surviving siblings, had depressed plasma and erythrocyte cholinesterase levels. Urinary 

4-nitrophenol was detected in three children. Clinical signs and symptoms were typical of organophosphate toxicity, as described in Section 3.2.1.4, with respiratory arrest as the terminal event (Dean et 

al. 1984). 

Death from a combination of inhalation and dermal exposures has been reported by Fazekas (1971) in 

four individuals who used methyl parathion (Wofatox) spray in a careless manner. These individuals 

were part of a larger series of 30 cases (20 men, 10 women) of fatal methyl parathion intoxication 

reported by Fazekas (1971). Since 26 of these fatalities followed oral exposure, this report is discussed in 

detail in Sections 3.2.2.1 and 3.2.2.2. 

The LC50 values of methyl parathion have been established in rats. A 1-hour LC50 of 200 mg/m3

 and a 

4-hour LC50 of 120 mg/m3

 for males were determined by Kimmerle and Lorke (1968). One-hour LC50 

values of 257 mg/m3 for male rats and 287 mg/m3 for female rats were determined for 70–80% pure 

methyl parathion by EPA (1978e); the rats were exposed to aerosols of respirable size. Survivors of toxic 

doses recovered clinically by 10–14 days postexposure. Sex-related differences in acute mortality of 

rodents have also been observed after exposure to methyl parathion by other routes (Murphy and Dubois 

1958). 

The LC50 value for male rats for the acute-duration category is recorded in Table 3-1 and plotted in 

Figure 3-1. 


 

 

 

METHYL PARATHION 24 

3. HEALTH EFFECTS 

3.2.1.2 Systemic Effects 

No studies were located regarding gastrointestinal, hematological, musculoskeletal, or dermal effects in 

humans or animals after inhalation exposure to methyl parathion. Dean et al. (1984) reported that seven 

children exposed to methyl parathion by many routes exhibited pinpoint pupils, abdominal pain, and 

diarrhea. The respiratory, cardiovascular, hepatic, and renal effects reported by Fazekas (1971) that were 

found in humans acutely exposed to methyl parathion intoxication resulted from exposure by all three 

routes; however, the results did not distinguish between the routes. 

Respiratory Effects. Pulmonary edema was reported in humans dying from acute methyl parathion 

(Wofatox) intoxication (Fazekas 1971). Edema was found in a man who died 2 hours after intoxication, 

and, in other cases, edema was found in others who died as long as 9 days after exposure. Bronchoconstriction and hypersecretion of bronchial glands (bronchorrhea) are primary muscarinic effects of 

methyl parathion. The broncoconstriction, bronchorrhea, and bradycardia caused by methyl parathion are 

strongly conducive to pulmonary edema. 

Rats exposed to a 1-hour LC50 of methyl parathion (see Section 3.2.1.1) had moderate pulmonary 

congestion, hemorrhage, and edema (EPA 1978e). While these lesions could represent an irritant effect 

of inhaled aerosols of methyl parathion, they also may be secondary to agonal death, meaning resulting 

from the death process, or to muscarinic effects as noted in the previous paragraph. 

Cardiovascular Effects. Lesions in the heart and blood vessels have been reported in humans 

acutely intoxicated with methyl parathion (Wofatox) (Fazekas 1971) and are discussed in Section 3.2.2.2. 

However, many of these lesions may be secondary to the effects of methyl parathion on the conduction 

system of the heart, to other components ingested, or to therapeutic regimens that some of these patients 

received. 

Thymic hemorrhage and congested cerebral blood vessels occurred in rats exposed to a 1-hour LC50 of 

methyl parathion described in Section 3.2.1.1 (EPA 1978e). These are probably nonspecific agonal 

lesions. 

Hepatic Effects. Liver lesions were reported in humans dying of acute methyl parathion (Wofatox) 

intoxication (Fazekas 1971). See Section 3.2.2.2 for a description of these lesions. The hepatic effects 
 

 

METHYL PARATHION 25 

3. HEALTH EFFECTS 

were nonspecific and were likely a reflection of systemic effects of hypoxia, stress, therapeutic agents, or 

a combination of all of these. 

No studies were located regarding hepatic effects in animals after inhalation exposure to methyl 

parathion. 

Renal Effects. Kidney lesions were reported in humans dying of acute methyl parathion (Wofatox) 

intoxication (Fazekas 1971). See Section 3.2.2.2 for a description of these lesions. 

No studies were located regarding renal effects in animals after inhalation exposure to methyl parathion. 

Ocular Effects. One study reported that seven children exposed to methyl parathion by inhalation, 

oral, and possibly dermal routes exhibited pinpoint pupils (miosis) (Dean et al. 1984). This effect is a 

consequence of the effects on the autonomic nervous system. No other studies were located regarding 

ocular effects in humans or animals after inhalation exposure to methyl parathion. 

3.2.1.3 Immunological and Lymphoreticular Effects 

No studies were located regarding immunological effects in humans or animals after inhalation exposure 

to methyl parathion. 

3.2.1.4 Neurological Effects 

Neurological effects related to cholinesterase depression occurred in seven children acutely exposed to 

methyl parathion by inhalation as well as orally and dermally (Dean et al. 1984). The children were 

admitted to a local hospital with signs and symptoms of lethargy, increased salivation, increased 

respiratory secretions, and miosis. Two of the children were in respiratory arrest. Two children died 

within several days of each other. All of the children had depressed plasma and erythrocyte 

cholinesterase levels (Table 3-2). These effects are similar to those occurring in methyl parathion 

intoxication by other routes (see Sections 3.2.2.4 and 3.2.3.4). Three adults exposed in the same incident 

had normal plasma (apart from one female) and red blood cell cholinesterase, and urinary levels of 

4-nitrophenol (0.46–12.7 ppm) as high as some of the ill children. 
METHYL PARATHION 26 

3. HEALTH EFFECTS 

Table 3-2. Plasma and Erythrocyte Cholinesterase Levels in Children
 

Intoxicated by Methyl Parathiona
 

Plasma cholinesterase Erythrocyte cholinesterase 

Age/sex (mU per mL per minute)b (∆pH/hour)c 

11 years/female (died) No data No data

 9 years/male 1,023 0.15

 8 years/male 987 0.10

 6 years/female 1,707 0.10

 5 years/female 964 0.10

 4 years/female (died) 914 0.00

 2 years/female 1,534 0.10 

a

Adapted from Dean et al. 1984

b

Normal value: 2,450–4,850 

c

Normal value: 0.57–0.98 

∆ = change; mU = milliunits; mL = milliliter 
METHYL PARATHION 27 

3. HEALTH EFFECTS 

Male rats exposed to 264 mg/m3 of methyl parathion by inhalation had 59% (range: 53–61%) inhibition 

of blood (a combination of erythrocyte and plasma) cholinesterase 1 hour after exposure (EPA 1978e). 

These animals had typical cholinergic signs of toxicity: salivation, exophthalmos, lacrimation, 

spontaneous defecation and urination, and muscle fasciculation. Values for controls were not provided. 

Death was not correlated to the degree of cholinesterase inhibition in whole blood. 

3.2.1.5 Reproductive Effects 

No studies were located regarding reproductive effects in humans or animals after inhalation exposure to 

methyl parathion. 

3.2.1.6 Developmental Effects 

No studies were located regarding developmental effects in humans or animals after inhalation exposure 

to methyl parathion. 

3.2.1.7 Cancer 

No studies were located regarding carcinogenic effects in humans or animals after inhalation exposure to 

methyl parathion. 

3.2.2 Oral Exposure 

3.2.2.1 Death 

There have been a number of cases of human intoxication and death from oral exposure to methyl 

parathion. 

Two of seven children who ingested methyl parathion in contaminated drinking water, and also were 

exposed by inhalation and possibly by dermal contact following spraying of methyl parathion inside a 

house, died (Dean et al. 1984). Additional details are provided in Section 3.2.1.1. 

A 50-year-old white male died after intentional methyl parathion ingestion (Wofatox liquid) (Fazekas and 

Rengei 1964). The estimated dose of methyl parathion was 1,840 mg. Gross necropsy findings consisted 
METHYL PARATHION 28 

3. HEALTH EFFECTS 

of congested cerebral meninges, brain edema, generalized visceral congestion, laryngeal and pulmonary 

edema, fatty liver, intense congestion of the esophageal mucosa, and petechial hemorrhages on the 

mucosa of the stomach and intestines. Histopathologic examination of tissues was not performed. The 

estimated dose of 1,840 mg methyl parathion corresponds to a bolus dose of 26 mg/kg. None of the 

reported autopsy findings are specific to organophosphate intoxication. A lethal oral dose of 307–660 mg 

has been reported for adults (Fazekas and Rengei 1964). 

Thirty fatalities, 20 men and 10 women, resulted from acute exposure to methyl parathion (Wofatox) 

(Fazekas 1971). Patients ranged in age from 18 to 82 years. They died between 2 hours and 9 days after 

exposure to Wofatox. A number of these individuals received intensive therapy but died nonetheless. Of 

the 30 cases, 26 had intentionally ingested 50–300 g of Wofatox, while the rest had a combination of 

excessive dermal and inhalation exposure during spraying. Histological lesions were reported in liver, 

kidney, spleen, heart, brain, and vascular endothelium. Lesions were not categorized by exposure route. 

These lesions are described in Section 3.2.2.2 under the various organ systems and in Section 3.2.2.4 

under neurological effects. Most of these lesions are not specific for methyl parathion in particular or 

organophosphates in general. 

Numerous studies in experimental animals have established LD50 values for acute oral exposure to methyl 

parathion. In most of these studies, technical grade, purified methyl parathion, or an emulsion 

concentration (EC) formulation was administered by gavage in a vehicle such as propylene glycol. 

Species tested were rats (EPA 1978e; Gaines 1960; Miyamoto et al. 1963b; Sonnenschein et al. 1989b; 

Yamamoto et al. 1982), mice (El-Herrawie and El-Sayed 1986; Haley et al. 1975b; Metcalf and March 

1953; Miyamoto et al. 1963b), and guinea pigs (Miyamoto et al. 1963b). 

In rats, the LD50 for males tended to be lower, although not statistically significantly different, in 

comparison with that for females (EPA 1978e; Gaines 1960). In CD-1 mice, males had a significantly 

lower LD50 than did females (Haley et al. 1975b). Similar sex-related differences have been seen with 

some other thio-organophosphate pesticides and were attributed to more efficient conversion of these 

compounds to their active paraoxon metabolites in the liver of males (Murphy and DuBois 1958). 

The LD50 values for methyl parathion were compared to those for methyl paraoxon, the active metabolite 

of methyl parathion, in rats, guinea pigs, and mice by Miyamoto et al. (1963b). Methyl paraoxon was 

5.4 times more potent than methyl parathion in male rats, 5 times more potent in male guinea pigs, and 

1.6 times more potent in mice. 
METHYL PARATHION 29 

3. HEALTH EFFECTS 

In mice, heat-induced isomers of purified methyl parathion were less lethal than was purified methyl 

parathion alone (LD50 of >200 mg/kg for heat-induced isomers compared to 100–200 mg/kg for methyl 

parathion) (Metcalf and March 1953). Eighty-five percent of the sample was heat-isomerized, but the 

isomers were not precisely identified. Methyl parathion in an emulsifiable concentrate had greater acute 

(24 hours) oral lethality for male mice than it did in the technical or microencapsulated formulations. For 

microencapsulated methyl parathion, the toxicity of the supernatant increased over storage time from an 

LD50 value of 21.2 mg/kg before storage to 14.9 mg/kg at 2 months storage time, indicative of gradual 

release of methyl parathion from the capsules to the liquid during storage (El-Herrawie and El-Sayed 

1986). 

Clinical signs of acute oral toxicity of methyl parathion and methyl paraoxon were characterized by 

Miyamoto et al. (1963b) in rodents. Signs occurred within minutes after compound administration and 

consisted of dyspnea, twitching, clonic convulsions, salivation, chromodacryorrhea, and exophthalmos. 

The signs lasted for 30–60 minutes, at which time death usually occurred. However, guinea pigs tended 

to develop less severe signs, and deaths occurred up to 24 hours postdosing. 

An 8-week dietary study of methyl parathion was performed by NCI (1979) in order to select doses for a 

chronic bioassay. F344 rats of both sexes (five animals/sex/group) received doses of 0, 0.5, 1, 1.5, 2, or 

2.5 mg/kg/day. B6C3F1 mice (five animals/sex/group) received doses of 0, 2.6, 5.2, 7.8, 10.4, 13, 16.2, 

32.5, or 65 mg/kg/day. All male rats survived to study termination. One of five females fed 0.5, 1.5, and 

2 mg/kg/day and two of five females fed 2.5 mg/kg/day died. In mice, significant mortality occurred at 

the two highest doses; all males died in the 32.5- and 65-mg/kg/day groups, as did all females in the 

65-mg/kg/day group. Clinical signs in both sexes in the 32.5- and 65-mg/kg/day dosage groups were 

rough hair coat and arched back. The results suggest that male mice may be more susceptible than 

females to intermediate-duration exposure, in contrast to the acute lethality data for mice and to the 

results for rats in this intermediate-duration study. 

All reliable lethal doses (LD50 values) for each species and for the acute- and intermediate-duration 

categories are recorded in Table 3-3 and plotted in Figure 3-2. 

3.2.2.2 Systemic Effects 

Reductions in erythrocyte and plasma cholinesterase levels are considered biomarkers of neurological 

effects and not hematological effects as discussed in Sections 3.2.2.4 and 3.5.2. 













 

 

METHYL PARATHION 43 

3. HEALTH EFFECTS 

The highest NOAEL and the reliable LOAEL values for each systemic effect in each species and duration 

category are recorded in Table 3-3 and plotted in Figure 3-2. 

Respiratory Effects. Pulmonary edema has been reported in humans who died of acute methyl 

parathion (Wofatox) intoxication (Fazekas 1971). Edema was found in a man who died 2 hours after 

intoxication and in others who died as long as 9 days after exposure. Bronchoconstriction and hypersecretion of bronchial glands are primary muscarinic effects of methyl parathion. Pulmonary edema is 

not considered to be a primary effect of methyl parathion; it is considered to be secondary to the 

neurologic effects of this compound on the heart and vascular smooth muscle. 

Routine gross and histopathological examinations revealed no treatment-related effects on the respiratory 

system of dogs exposed to 0.03, 0.1, or 0.3 mg/kg/day methyl parathion in the diet for 1 year (Suba 

1981). Chronic dietary exposure to methyl parathion did not induce respiratory effects in mice fed 

16.2 mg/kg/day or rats fed 2 mg/kg/day (NCI 1979). 

Cardiovascular Effects. Cardiovascular lesions were reported in some of the 30 cases of acute fatal 

intoxication by methyl parathion studied by Fazekas (1971). Patients who survived at least 20–24 hours 

had degeneration of the heart muscle with segmentation, fragmentation, and splitting of myofibers. 

Vascular lesions were congestion and multifocal hemorrhages in the central nervous system and in 

visceral organs. Patients surviving 28 hours to 9 days after intoxication (and receiving intensive therapy) 

had widespread swelling of vascular endothelium with areas of desquamation into vessel lumens. Blood 

vessel walls and perivascular spaces were edematous. However, many of these lesions may be secondary 

to the effects of methyl parathion on the conduction system of the heart, to other components ingested, or 

to therapeutic regimens that some of these patients received. 

Rats exposed by gavage to 19 mg/kg (LD50 dose) or 9.5 mg/kg (half of the LD50 dose) of methyl parathion 

developed abnormalities in their heart rate and electrocardiograms (Galal et al. 1975). Bradycardia was 

observed in both groups 1 and 2 hours after oral introduction of the methyl parathion (85% reduction in 

rate in the LD50 group and 68% reduction in the one-half-LD50 group). Severe arrhythmia and electrocardiographic abnormalities suggestive of myocardial ischemia also occurred. In comparison to 

malathion and carbaryl, methyl parathion produced the greatest cardiotoxic changes. 

A significant increase in heart-to-body-weight ratio occurred in female rats exposed to 2.5 mg/kg/day 

methyl parathion in the diet for 2 years, but not in rats exposed to either 0.025 or 0.25 mg/kg/day methyl 
 

 

METHYL PARATHION 44 

3. HEALTH EFFECTS 

parathion (Suba 1984). This effect did not have any complementary histopathology. Routine gross and 

histopathological examinations revealed no treatment-related effects on the cardiovascular system of dogs 

exposed to 0.03, 0.1, or 0.3 mg/kg/day methyl parathion in the diet for 1 year (Suba 1981). Chronic 

dietary exposure to methyl parathion did not induce cardiovascular effects in mice fed 16.2 mg/kg/day or 

rats fed 2 mg/kg/day (NCI 1979). 

Gastrointestinal Effects. Intense congestion of the esophageal mucosa and petechial hemorrhages 

in the stomach and intestine were reported in a patient who committed suicide by ingesting methyl 

parathion (Wofatox) (Fazekas and Rengei 1964). In a series of 30 cases of methyl parathion (Wofatox) 

fatalities, inflammation was present in the stomach and intestine at autopsy (Fazekas 1971). These 

victims died within 2 hours to 9 days after exposure, even after intensive therapy. All these gastrointestinal findings are nonspecific and cannot be attributed to a primary effect of methyl parathion. 

In an 8-week study to establish doses for a chronic dietary bioassay of methyl parathion, B6C3F1 mice 

received dietary methyl parathion at levels of 0, 2.6, 5.2, 7.8, 10.4, 13, 16.3, 32.5, and 65 mg/kg/day. 

Gastric hemorrhage was present at necropsy in five of five males receiving 32.5 mg/kg/day and in three of 

five males and five of five females receiving 65 mg/kg/day (NCI 1979). This finding was correlated with 

mortality (see Section 3.2.2.1). Routine gross and histopathological examinations revealed no treatmentrelated effects on the gastrointestinal system of dogs exposed to 0.03, 0.1, or 0.3 mg/kg/day methyl 

parathion in the diet for 1 year (Suba 1981). Chronic dietary exposure to methyl parathion did not induce 

gastrointestinal effects in mice fed 16.2 mg/kg/day or rats fed 2 mg/kg/day (NCI 1979). 

Hematological Effects. No studies were located regarding hematological effects in humans after 

oral exposure to methyl parathion. 

Total leukocyte and differential cell counts were not affected in female mice given 6 mg/kg/day of methyl 

parathion by gavage for 28 days (Crittenden et al. 1998). In male rats administered methyl parathion by 

gavage at doses of 0.218, 0.436, or 0.872 mg/kg/day for 28 days, the two highest dose groups exhibited 

dose-related significant decreases in mean corpuscular volume. No significant dose-related changes were 

seen in red blood cell count or absolute and differential white blood cell counts (Undeger et al. 2000). An 

additional intermediate-duration study in rats reported anemia (decreased hematocrit and erythrocyte 

count) and slight leukocytosis with neutropenia and lymphocytosis following treatment with an 

undetermined dose of methyl parathion, but higher than 0.37 mg/kg/day (Galal et al. 1977); this study is 

not presented in Table 3-2. Mean hemoglobin, hematocrit, and erythrocyte counts were significantly 
 

 

METHYL PARATHION 45 

3. HEALTH EFFECTS 

reduced in female rats at 6–24 months of exposure to 2.5 mg/kg/day methyl parathion, which was given 

in the diet for 2 years (Suba 1984). Mean hematocrit and erythrocyte counts were significantly reduced in 

males at 24 months of exposure to either 0.25 or 2.5 mg/kg/day methyl parathion. These effects did not 

occur in rats exposed to 0.025 mg/kg/day methyl parathion. A NOAEL of 0.025 mg/kg/day was 

identified from these data. Based on this value, a chronic oral MRL of .0003 mg/kg/day was calculated as 

described in the footnote in Table 3-3. No treatment-related effects were noted following routine 

hematological testing in dogs exposed to 0.03, 0.1, or 0.3 mg/kg/day methyl parathion in the diet for 

1 year (Suba 1981). 

Musculoskeletal Effects. No studies were located regarding musculoskeletal effects in humans after 

oral exposure to methyl parathion. 

Routine gross and histopathological examinations revealed no treatment-related effects on the musculoskeletal system of dogs exposed to 0.03, 0.1, or 0.3 mg/kg/day methyl parathion in the diet for 1 year 

(Suba 1981). Chronic dietary exposure to methyl parathion did not induce musculoskeletal effects in 

mice fed 16.2 mg/kg/day or rats fed 2 mg/kg/day (NCI 1979). 

Hepatic Effects. Liver lesions have been reported in humans acutely intoxicated by methyl parathion 

formulation (Wolfatox) (Fazekas 1971; Fazekas and Rengei 1964). These studies are discussed in detail 

in Section 3.2.2.1. Liver lesions were hepatocellular swelling, degeneration, and fatty change. 

Intoxicated patients surviving for 28 hours to 9 days had hepatocytes free in central or hepatic veins; this 

finding was described as mobilization of liver cells. The role of methyl parathion in the induction of all 

of these lesions is unclear. 

Rats were given one or two LD50 doses of methyl parathion, spaced 14 days apart (Sonnenschein et al. 

1989b). Male rats had elevated serum alanine aminotransferase indicative of hepatocellular damage. The 

enzyme levels returned to normal within 48 hours after exposure. Serum levels of tyrosine aminotransferase, an enzyme induced in liver by glucocorticoids, also increased. Liver lesions were more 

severe after the second dose of methyl parathion. They consisted of single cell necrosis of hepatocytes, 

hepatocellular swelling, binucleate hepatocytes, rare fatty vacuolization of hepatocytes, and Kupffer cell 

proliferation (Sonnenschein et al. 1989a). These changes may be secondary, stress-related findings rather 

than direct toxic effects of methyl parathion. 
 

 

 

METHYL PARATHION 46 

3. HEALTH EFFECTS 

Routine gross and histopathological examinations revealed no treatment-related effects on the hepatic 

system of dogs exposed to 0.03, 0.1, or 0.3 mg/kg/day methyl parathion in the diet for 1 year (Suba 

1981). Chronic dietary exposure to methyl parathion did not induce hepatic effects in mice fed 

16.2 mg/kg/day or rats fed 2 mg/kg/day (NCI 1979). 

Renal Effects. Acute nephrosis has been reported in humans after acute, lethal intoxication (Fazekas 

1971) by methyl parathion (Wofatox). This may be a secondary effect of hypoxia related to the 

neurologic effects of methyl parathion on vascular smooth muscle and on the electrical conduction system 

of the heart. It could also be related to therapeutic efforts. 

Routine gross and histopathological examinations revealed no treatment-related effects on the renal 

system of dogs exposed to 0.03, 0.1, or 0.3 mg/kg/day methyl parathion in the diet for 1 year (Suba 

1981). Chronic dietary exposure to methyl parathion did not induce renal effects in mice fed 

16.2 mg/kg/day or rats fed 2 mg/kg/day (NCI 1979). 

Dermal Effects. No studies were located regarding dermal effects in humans after oral exposure to 

methyl parathion. 

Routine gross and histopathological examinations revealed no treatment-related dermal effects on dogs 

exposed to 0.03, 0.1, or 0.3 mg/kg/day methyl parathion in the diet for 1 year (Suba 1981). 

There was an increased incidence of alopecia in female rats treated for 2 years with 2.5 mg/kg/day methyl 

parathion compared to either vehicle controls, high-dose males, or rats treated with either 0.025 or 

0.25 mg/kg/day methyl parathion (Suba 1984). Chronic dietary exposure to methyl parathion did not 

induce dermal effects in mice fed 16.2 mg/kg/day or rats fed 2 mg/kg/day (NCI 1979). 

Ocular Effects. One study reported that seven children exposed to methyl parathion by inhalation, 

oral, and possibly dermal routes exhibited pinpoint pupils (miosis) (Dean et al. 1984). This effect is a 

consequence of the effects on the parasympathetic nervous system. No other studies were located 

regarding ocular effects in humans after oral exposure to methyl parathion. 

There were no treatment-related effects on retinal function and no morphological effects on the eyes of 

dogs that were exposed to 0.03, 0.30, or 3.00 mg/kg/day methyl parathion for 13 weeks and allowed 

4 weeks of no exposure to recover (Daly 1989). 
 

METHYL PARATHION 47 

3. HEALTH EFFECTS 

Routine gross and histopathological examinations revealed no treatment-related effects on the ocular 

systems of dogs exposed to 0.03, 0.1, or 0.3 mg/kg/day methyl parathion in the diet for 1 year (Suba 

1981). 

Female rats exposed to 2.5 mg/kg/day methyl parathion exhibited retinal degeneration, which was noted 

at 24 and 28 months but not at 3 or 12 months of a 2-year treatment (Suba 1984). Posterior subcapsular 

cataracts also occurred in the high-dose females and may be related to retinal degeneration. These data 

are limited because the incidence of the effects was not reported with respect to controls or other treated 

groups and the statistical significance was not determined. The incidence of bilateral retinal atrophy was 

significantly greater in female rats that were chronically exposed to 2.5 mg/kg/day methyl parathion than 

in vehicle controls (Suba 1984). This effect was not significant in rats exposed to either 0.025 or 

0.25 mg/kg/day methyl parathion. Chronic dietary exposure to methyl parathion did not induce ocular 

effects in mice fed 16.2 mg/kg/day or rats fed 2 mg/kg/day (NCI 1979). 

Body Weight Effects. No effect on body weight was seen in mice administered 5 mg/kg/day of 

methyl parathion by gavage for 15 days (Tian et al. 1997). Body weight gain in male rats was not 

affected by oral (gavage) administration of methyl parathion at 0.872 mg/kg/day for 28 days (Undeger et 

al. 2000). No effect on body weight gain was seen in male rats whose dams were administered 

0.88 mg/kg/day during days 5–15 of gestation and from day 2 after delivery through weaning of the pups, 

which were then continued on the same doses for 8 weeks (Desi et al. 1998). Emaciation and dehydration 

were noted in two of eight male dogs treated with 3.00 mg/kg/day methyl parathion for 13 weeks in the 

diet, but not in dogs treated with either 0.03 or 0.30 m7g/kg/day methyl parathion (Daly 1989). These 

effects were reported to be due to treatment with methyl parathion, although the statistical significance of 

the effects was not determined. Also, male dogs treated with 3.00 mg/kg/day methyl parathion had a 

30% decrease in body weight gain compared to controls. The other treatment groups did not exhibit this 

effect. There were no significant effects on mean body weights in any of the treatment groups. 

Male and female rats exposed to 2.5 mg/kg/day methyl parathion in the diet for 2 years had statistically 

significant reduced body weights when compared to vehicle controls (Suba 1984). This effect was not 

consistent throughout the study and did not occur in rats exposed to either 0.025 or 0.25 mg/kg/day 

methyl parathion. Mean food consumption values were significantly elevated in male rats but only within 

the first 13 weeks of the 2-year exposure to 2.5 mg/kg/day methyl parathion (Suba 1984). Females 

exposed to 2.5 mg/kg/day methyl parathion had significantly reduced food intake values during the first 

2 weeks of exposure, but intake was significantly elevated from week 3 to termination. Effects on food 
 

METHYL PARATHION 48 

3. HEALTH EFFECTS 

consumption did not occur in rats exposed to 0.025 or 0.25 mg/kg/day methyl parathion. There were no 

treatment-related effects on body weight or food intake in dogs that were exposed to either 0.03, 0.1, or 

0.3 mg/kg/day methyl parathion in the diet for 1 year (Suba 1981). Also, no such effects were noted 

following chronic dietary exposure to methyl parathion in mice fed 16.2 mg/kg/day or rats fed 

2 mg/kg/day (NCI 1979). 

Other Systemic Effects. Female rats, but not males, treated with 2.5 mg/kg/day methyl parathion 

had greater frequency of yellow ano-genital staining than the control females or females treated with 

either 0.025 or 0.25 mg/kg/day methyl parathion (Suba 1984). 

3.2.2.3 Immunological and Lymphoreticular Effects 

No studies were located regarding immunological effects in humans after oral exposure to methyl 

parathion. 

An increased ratio of T suppressor cells to T helper cells was seen in mice given 2.5 and 5.0 mg/kg/day of 

methyl parathion for 15 days; the spleen to body weight ratio was increased at 5 mg/kg/day (Tian et al. 

1997). No other immunological or lymphoreticular end points were measured. 

In female mice administered methyl parathion by gavage at doses of 1, 3, or 6 mg/kg/day for 28 days or 

6 mg/kg/day for 7, 14, 21, or 28 days, natural killer cell activity was increased at 1 and 3 mg/kg/day (but 

not at 6 mg/kg/day at any duration) (Crittenden et al. 1998). Peritoneal macrophage activity was 

increased at all three doses, and cytotoxic T lymphocyte activity was not affected. Spleen cellularity (but 

not spleen weight) was increased at 7–21 days, but decreased at 28 days in mice receiving 6 mg/kg/day. 

The number of splenic plaque-forming cells following in vitro challenge with sheep red blood cells was 

decreased at all three doses of methyl parathion, in a dose-related manner. No decrease in antibody 

production was seen, however, when the mice were immunized with sheep red blood cells in vivo during 

methyl parathion treatment. Resistance to melanoma cells and to group b streptococci was not affected 

by methyl parathion. The results, taken together, do not indicate a serious decrement in immune function 

at these doses, which produced no overt cholinergic signs. 

There was a suggestion of dose-related immunosuppressive effects in rabbits fed methyl parathion in the 

diet at 0.04, 0.16, 0.57, and 1.48 mg/kg/day for 4 weeks. These effects consisted of decreased numbers of 

plasma cells in popliteal lymph nodes (at all doses compared to controls), decreased numbers of germinal 
METHYL PARATHION 49 

3. HEALTH EFFECTS 

centers in splenic white pulp, and atrophy of thymic cortical tissue (only at 0.57 mg/kg/day) (Street and 

Sharma 1975). Humoral immunity to NIISI typhoid vaccine was inhibited in rats given 1.25 mg/kg/day 

methyl parathion. This effect was noted when vaccination occurred prior to or during the 35–50-day 

period of exposure to methyl parathion (Shtenberg and Dzhunusova 1968). 

The effects on the immune system may be related to stress (glucocorticoid) rather than a direct effect of 

methyl parathion, although a stress-related effect is more likely for neurotoxic doses (Kunimatsu et al. 

1996). 

No significant changes in immune function parameters (IgM-plaque forming cells assay, delayed-type 

hypersensitivity reaction) were observed in rats administered methyl parathion by gavage at doses of 

0.218, 0.436, or 0.872 mg/kg/day for 28 days (Undeger et al. 2000). Routine gross and histopathological 

examinations revealed no treatment-related effects on the immune system of dogs exposed to 0.03, 0.1, or 

0.3 mg/kg/day methyl parathion in the diet for 1 year (Suba 1981). 

The reliable LOAEL values for immunological effects in rats for the intermediate-duration category and 

the highest NOAEL in dogs for the chronic-duration category are recorded in Table 3-3 and plotted in 

Figure 3-2. 

3.2.2.4 Neurological Effects 

Neurological effects related to cholinesterase depression occurred in seven children acutely exposed to 

methyl parathion by inhalation as well as orally and dermally (Dean et al. 1984). See Section 3.2.1.4 for 

additional details. 

Neurologic signs and symptoms developed in 26 humans after intentional lethal intoxication by methyl 

parathion (Wofatox) via the oral route (Fazekas 1971). A number of the patients studied had considerable 

reduction (values not specified) in plasma cholinesterase activity. Typical signs and symptoms of 

intoxication by methyl parathion or other organophosphates are described in Section 3.5. Reductions in 

erythrocyte or plasma cholinesterase levels did not occur after two male university faculty volunteers 

ingested 2 mg/day of methyl parathion for 5 days and again 1–8 weeks later ingested 4 mg/day for 5 days 

(Rodnitzky et al. 1978). Neurobehavioral changes, as measured by a battery of tests, also did not occur. 

The subjects’ predosing test values were the only controls for this study. 
METHYL PARATHION 50 

3. HEALTH EFFECTS 

Neurologic signs did not occur over a 30-day period in male prisoner volunteers in California who 

ingested daily doses of methyl parathion ranging from 1.0 to 19 mg. There were no uniform changes in 

plasma or erythrocyte cholinesterase levels at any of these doses (Rider et al. 1969). By increasing 

concentrations of methyl parathion administered to the same experimental population and using the same 

protocol, a dose that inhibited cholinesterase values was established. These additional studies were 

published nearly 20 years ago in abstract form only; therefore, they are not discussed in this section. 

Neurologic signs occurred in animals following oral exposure to methyl parathion at doses that caused 

reductions in erythrocyte, brain, and/or plasma cholinesterase levels. Male rats receiving 5 mg/kg orally 

by gavage developed cholinergic signs 7 minutes after dosing, with convulsions beginning within 

16 minutes. Plasma cholinesterase was reduced to 43.6% of control levels (Youssef et al. 1987). Rats 

given methyl parathion by gavage at doses of 4 or 8 mg/kg/day developed cholinergic signs, and all rats 

died within 4 days. A single oral dose of 13 mg/kg or repeated doses of 1.3 mg/kg/day for 10 days 

induced significant inhibition of plasma and brain cholinesterase levels, with brain levels being 43% of 

the control value after the single dose and 56% of the control value after the repeated lower doses 

(Yamamoto et al. 1982). 

When methyl parathion was given orally to rats at doses of 1.5 mg/kg and to guinea pigs at 50 mg/kg, 

plasma, erythrocyte, and brain cholinesterase activity was maximally inhibited within 30 minutes after 

administration. In rodents of both species that died after acute intoxication, brain cholinesterase levels 

decreased to 20% of control values and often to 5–7% (Miyamoto et al. 1963b). The species difference in 

susceptibility to orally administered methyl parathion is noted in Section 3.2.2.1. 

Following acute oral toxicity from dosages ranging from 14 to 80 mg/kg, laboratory rats had earlier 

recovery of brain acetylcholinesterase levels than did feral cotton rats. Similar results were seen in a 

comparison of laboratory mice to feral mice (Roberts et al. 1988). 

No cholinergic signs were seen in mice administered 6 mg/kg/day for 7–28 days (Crittenden et al. 1998). 

Brain acetylcholinesterase was significantly decreased at 3 and 6 (but not 1) mg/kg/day, and plasma 

cholinesterase was significantly decreased at 6 mg/kg/day. 

Pregnant rats given methyl parathion orally at 1.5 mg/kg/day from day 6 to day 15 or 19 of gestation had 

cholinergic effects (Gupta et al. 1984). These effects were not seen at 1 mg/kg/day. Similarly, pregnant 

rats given methyl parathion orally at 1.5 mg/kg/day from day 6 through day 20 of gestation had 
METHYL PARATHION 51 

3. HEALTH EFFECTS 

cholinergic signs, but those given 1 mg/kg/day did not (Gupta et al. 1985). At both dose levels, the dams 

had significant and dose-related depression of brain acetylcholinesterase activity and nondose-related 

decreases in brain muscarinic receptors. Effects in the fetuses and offspring are discussed in 

Section 3.2.2.5. 

A study of three pesticides, administered separately, reported electrophysiological effects in male rats 

treated with methyl parathion through gavage administration to their dams during days 5–15 of gestation 

and days 2–28 of lactation at doses of 0.22, 0.44, or 0.88 mg/kg/day, followed by direct treatment of the 

male offspring in the same manner for 8 weeks, from weaning through 11–12 weeks of age. Dose-related 

changes on electrocorticograms of the somatosensory, visual, and auditory centers, on evoked potentials, 

and on tail nerve conduction velocity and refractory period were observed (Desi et al. 1998). The results 

were stated to be significantly different from controls at all three dose levels, but results specifically for 

methyl parathion were shown only for the electrocorticogram of the somatosensory area. No overt signs 

of toxicity were seen in the offspring. A minimal LOAEL of 0.22 mg/kg/day was identified from these 

experiments in which the rats were treated starting in the prenatal period and continuing though 12 weeks 

of age. Based on this value, an intermediate oral MRL of .0007 mg/kg/day was calculated as described in 

the footnote in Table 3-3. 

In the same study (Desi et al. 1998), no significant effects on these end points were seen in male rats 

exposed to methyl parathion only through the treatment of their dams during gestation or gestation and 

lactation; these results are presented in Section 3.2.2.6. 

Dogs receiving 0.12, 0.5, or 1.2 mg/kg/day methyl parathion in their diet for 12 weeks had reduced 

erythrocyte cholinesterase levels: 65% of baseline values for the 0.5-mg/kg/day group and 60% of 

baseline values for the 1.2-mg/kg/day group (Williams et al. 1959). Cholinesterase values in dogs fed 

0.12 mg/kg/day in the diet did not differ significantly from controls. Over an 8-week postexposure 

period, the erythrocyte cholinesterase levels in dogs in the two highest dose groups recovered 

approximately 1% per day. Study limitations included the use of only two dogs (one of each sex) per 

dose group, use of dogs from unspecified sources, no discussion of clinical signs (if any), and no 

correlation of reduced cholinesterase values with general effects on the dogs' health. 

A dose-response relationship was noted in dogs exposed to 0.03, 0.3, or 3.0 mg/kg/day methyl parathion 

in the diet for 13 weeks (Daly 1989). Significant reductions in erythrocyte cholinesterase activity 

(20–23%) and cholinesterase activity in the pons and cerebellum of the brain (43–54%) occurred in dogs 
METHYL PARATHION 52 

3. HEALTH EFFECTS 

that were given 3.0 mg/kg/day methyl parathion for 13 weeks. There were no effects on either 

erythrocyte or brain cholinesterase activities in dogs that were given either 0.03 or 0.3 mg/kg/day methyl 

parathion. Significant reductions (53–59%) in plasma cholinesterase also occurred in the high-dose 

females. This latter effect was observed in both low- and high-dose males, but not in males at the mid 

dose. Thus, the results in the low-dose males do not appear to be treatment related. There were no effects 

on cholinesterase activity in any of the exposure groups following a 30-day postexposure recovery period. 

Routine gross and histopathological examinations revealed no treatment-related effects on the nervous 

system of dogs exposed to 0.03, 0.1, or 0.3 mg/kg/day methyl parathion in the diet for 1 year (Suba 

1981). In addition, there were no treatment-related effects on cholinesterase activity in plasma, red blood 

cells, or brains in dogs under these exposure conditions. These data are in agreement with the NOAEL 

established above for dogs exposed to these levels for 13 weeks. 

Slight tremor was noted during the first 3 weeks to 4 months of treatment in male and female rats that 

were exposed to 2.5 mg/kg/day methyl parathion for 2 years; however, this effect subsided as exposure 

continued (Suba 1984). This effect was not noted in rats exposed to either 0.025 or 0.25 mg/kg/day 

methyl parathion. Abnormal gait was consistently observed in 2–14 out of 60 of the high-dose female 

rats from week 19 to termination and in 1 high-dose male, but only at the beginning of the second year of 

exposure. In addition, one female exposed to 0.25 mg/kg/day exhibited this effect from week 77 until 

termination. This effect did not occur in the controls or the low-dose exposure group. The data are 

limited for each of these effects because statistical significance was not determined. Peripheral 

neuropathy of the proximal and distal sciatic nerve in male and female rats was found to be related to 

chronic exposure to 2.5 mg/kg/day methyl parathion but not to 0.025 or 0.25 mg/kg/day methyl parathion 

(Suba 1984). Methyl parathion did not induce histopathological effects in the brain or spinal cord of 

treated animals. The pathology data are limited because statistical significance was not determined. 

Mean plasma, erythrocyte, and brain cholinesterase activities were significantly reduced by 67–88%, 

9–20%, and 76–79%, respectively, in rats of both sexes following 2-year exposures to 2.5 mg/kg/day 

methyl parathion (Suba 1984). This effect did not occur in rats exposed to either 0.025 or 0.25 mg/kg/day 

methyl parathion. 

All reliable LOAEL values for neurological effects in rats for the acute-duration category, the highest 

NOAEL and all reliable LOAEL values in dogs for the intermediate-duration category, and the highest 
METHYL PARATHION 53 

3. HEALTH EFFECTS 

NOAEL and all reliable LOAEL values in dogs and rats for the chronic-duration category are recorded in 

Table 3-3 and plotted in Figure 3-2. 

3.2.2.5 Reproductive Effects 

No studies were located regarding reproductive effects in humans after oral exposure to methyl parathion. 

Methyl parathion has not been shown to be toxic to male germ cells in mice exposed to the chemical in 

the diet or drinking water in three studies discussed in Section 3.2.2.7. An additional study, also 

discussed in Section 3.2.2.7, reported significantly increased numbers of abnormal sperm in male mice 

administered methyl parathion by gavage at relatively high doses. Routine gross and histopathological 

examinations revealed no treatment-related effects on the reproductive system of dogs exposed to 0.03, 

0.1, or 0.3 mg/kg/day methyl parathion in the diet for 1 year (Suba 1981). 

The highest NOAEL value in dogs for reproductive effects for the chronic-duration category is recorded 

in Table 3-3 and plotted in Figure 3-2. 

3.2.2.6 Developmental Effects 

No studies were located regarding developmental toxicity in humans after oral exposure to methyl 

parathion. 

Placental transfer of methyl parathion was demonstrated following oral administration to pregnant rats 

1–3 days before parturition (Ackermann and Engst 1970). 

In a study of the effects of methyl parathion on protein synthesis, rats were given 1 mg/kg/day of methyl 

parathion in a small amount of peanut butter (eaten within 2 minutes) or 1.5 mg/kg methyl parathion by 

gavage in peanut oil starting on day 6 of gestation and continuing through day 15 or 19. These exposures 

inhibited incorporation of 14C valine into protein in maternal, placental, and fetal tissues (Gupta et 

al. 1984). A dose-related inhibition was observed in maternal brain, viscera, placenta, and whole embryos 

in rats on day 15 and in fetal brain and viscera on day 19. The inhibitory effect of methyl parathion on 

protein synthesis was greater on day 19 than on day 15 of gestation and was more pronounced in fetal 

than in maternal tissues. No signs of maternal toxicity were seen at 1 mg/kg/day. Signs of cholinergic 

stimulation, including muscle fasciculation, tremors, and mild clonic convulsions, were seen in some of 
METHYL PARATHION 54 

3. HEALTH EFFECTS 

the dams at 1.5 mg/kg/day, maternal body weight gains were slightly but significantly depressed, and 

resorptions were increased. No gross structural abnormalities were found in the fetuses. This study is 

limited in that it did not adequately examine whether reduction in protein synthesis during the prenatal 

period would cause adverse effects in the offspring. The purity of the compound was also not reported. 

In a follow-up study, pregnant rats were given 1 or 1.5 mg/kg/day of methyl parathion on days 6–20 of 

gestation (Gupta et al. 1985) in the same manner as in the previous study. Exposure to 1 mg/kg/day 

caused significant but small and transient reductions in maternal and fetal brain acetylcholinesterase 

activity, an increase in maternal but not fetal brain choline acetyltransferase activity, and a decease in 

maternal but not fetal muscarinic receptors. No visible signs of maternal or fetal toxicity were observed. 

Exposure to 1.5 mg/kg/day, on the other hand, significantly reduced acetylcholinesterase activity and 

increased choline acetyltransferase activity in the maternal brain and in all fetal brain regions at various 

stages during development. Muscarinic receptors were decreased in maternal but not fetal brains. Signs 

of cholinergic stimulation were seen in some of the dams. A slight but significant reduction in maternal 

weight gain and an increased incidence of fetal resorptions were also observed at 1.5 mg/kg/day. No 

gross structural abnormalities or changes in brain morphology were found in the fetuses. Impairment of 

behavior (decreased latency for cage emergence, reduction in accommodated locomotor activity, 

impairment of operant behavior) was found in 2–6-month-old offspring of rat dams fed methyl parathion 

at 1 mg/kg/day in peanut butter, but not in offspring of those administered 1.5 mg/kg/day in oil by 

gavage. The observed differences may have been caused by the differences in method and vehicle of 

administration, or potential nonlinearity in the dose-response for behavioral effects. Several other 

behavioral end points, measured in the offspring at various times from 1 day to 6 months of age, were not 

affected at either dose level. 

Similar results for rats were reported by Crowder et al. (1980). Oral administration of 1 mg/kg/day of 

methyl parathion (99.9% purity) in corn oil on days 7–15 of gestation resulted in increased mortality in 

pups, relative to controls. Significant difference from controls in a maze transfer test was observed in 

pups from the treated group. However, use of a single-dose level precluded the assessment of doseresponse, and several other behavioral end points were not affected. Furthermore, no information was 

presented regarding body weights or signs of toxicity in the treated dams. 

Gavage administration of 1.5 mg/kg/day of methyl parathion to rats on days 6–15 of gestation resulted in 

increased resorptions, decreased fetal body weight, and hemorrhagic spots in the brain ventricles and skin 
METHYL PARATHION 55 

3. HEALTH EFFECTS 

of the upper body of some of the fetuses (Kumar and Devi 1996). The data for hemorrhagic spots in the 

brain and skin were presented and analyzed for statistical significance as percent affected fetuses/total 

fetuses in dose group rather than percent per litter. Maternal toxicity (cholinergic signs and slight but 

significant depression of body weight gain) and significantly decreased placental weight and amniotic 

fluid weight were seen at 1.5 mg/kg/day. 

In a study of three pesticides, the 11–12-week-old male offspring of rat dams administered methyl 

parathion at 0.22, 0.44, or 0.88 mg/kg/day on days 5–15 of gestation by gavage in an aqueous vehicle had 

no statistically significant changes in electrocorticograms, evoked potentials, or tail nerve conduction 

velocity or refractory period (Desi et al. 1998). A similar lack of significant effect was seen in male 

offspring of dams treated in the same manner during gestation and from the second day after delivery 

until weaning of the offspring at 4 weeks of age. There were slight trends in these indices, consistent in 

direction with the results obtained when treatment of the offspring was continued after weaning (see next 

paragraph). The electrocorticograms and evoked potentials studied by Desi et al. (1998) are more 

sensitive than the behavioral end points studied by Gupta et al. (1984, 1985) and Crowder et al. (1980), 

the doses were similar (0.88 mg/kg/day versus 1 mg/kg/day), and the period between dosing and testing 

was similar. The above findings by Desi et al. (1998), therefore, do not corroborate the findings in the 

other two studies. Whether the exposure vehicle contributed to the different outcomes is uncertain. 

In the male offspring whose treatment was continued through 11–12 weeks of age, however, dose-related 

effects were seen on all the above end points, and these effects were significantly different from controls 

at all three dose levels (Desi et al. 1998) (see also Section 3.2.2.4). The study did not determine the 

critical period (if any) and duration of exposure for these neurological effects. A limitation of this study 

is that results specifically for methyl parathion were shown only for the somatosensory electrocorticogram; the other results for this chemical were stated in the text, but not shown. 

No dose-response relationship can be established for the developmental toxicity of methyl parathion from 

the available database. All reliable LOAEL values in rats for developmental effects for the acute- and 

intermediate-duration categories are recorded in Table 3-3 and plotted in Figure 3-2. 

3.2.2.7 Cancer 

No studies were located regarding carcinogenic effects in humans after oral exposure to methyl parathion. 
METHYL PARATHION 56 

3. HEALTH EFFECTS 

There are two studies that describe negative carcinogenesis of methyl parathion administered orally to 

rodents. Methyl parathion was given in the diet to F344 rats and B6C3F1 mice for 105 weeks (NCI 

1979). Methyl parathion dosages were as follows: 0, 1, and 2 mg/kg/day for rats; 0, 8, and 

16.2 mg/kg/day for female mice; and time-weighted average of 4.5 and 9.7 mg/kg/day for male mice. 

Time-weighted averages were used for male mice because methyl parathion dosages had to be adjusted 

downward after week 37 due to decreased mean body weight gain. A comprehensive set of tissues was 

examined by microscopy and gross necropsy. Study limitations included matched control groups for both 

species that were smaller (n=20) than methyl parathion dosage groups (n=50), dose adjustments during 

the study, and a significant increase in mortality in high-dose female rats (only 46% survived to study 

termination compared to 82% survival of low-dose females and 95% survival of control females). There 

were no lesions associated with the increased mortality. Under conditions of the bioassay, methyl 

parathion was not carcinogenic in rats or mice of either sex. Also, there were no noncancer systemic 

effects associated with methyl parathion exposure in rats or mice. In the second study, no treatmentrelated benign or malignant neoplasms were observed in rats following 2-year exposures to either 0.025, 

0.25, or 2.5 mg/kg/day methyl parathion in the diet (Suba 1984). 

3.2.3 Dermal Exposure 

3.2.3.1 Death 

Death in humans related to a combination of inhalation and dermal exposure was discussed in 

Sections 3.2.1.1 and 3.2.2.1. 

LD50 values for the dermal route of exposure to methyl parathion have been established in acute studies 

for rats: 67 mg/kg for males and females (Gaines 1960), 110 mg/kg for males, and 120 mg/kg for females 

(EPA 1978e). The LD50 in male mice exposed by dermal application of methyl parathion to their hind 

feet (rather than shaved backs) was 1,200 mg/kg (Skinner and Kilgore 1982a). The mice were muzzled to 

prevent oral exposure from grooming. 

The reliable LD50 values for rats and mice for the acute-duration category are recorded in Table 3-4. 

 

 

METHYL PARATHION 58 

3. HEALTH EFFECTS 

3.2.3.2 Systemic Effects 

No studies were located in humans or animals regarding respiratory, gastrointestinal, hematological, 

musculoskeletal, hepatic, or renal effects after dermal exposure to methyl parathion. 

Cardiovascular Effects. No studies were located in humans regarding cardiovascular effects after 

dermal exposure to methyl parathion. Rats exposed dermally to the LD50 of 67 mg of methyl parathion/kg 

or to a one-half-LD50 dose developed abnormalities in their heart rate and electrocardiograms (Galal et 

al. 1975). Bradycardia occurred by 1 hour after dosing with a severe effect at 2 hours after dosing 

(91% reduction in rate in the LD50 group and 70% reduction in rate in the one-half-LD50 group). 

Arrhythmia and electrocardiographic abnormalities were pronounced in rats receiving the dermal LD50 

dose of methyl parathion. 

Dermal Effects. Based on a skin patch test, allergic (contact) dermatitis to methyl parathion occurred 

in a farmer (Lisi et al. 1987). 

No studies were located regarding dermal effects in animals after dermal exposure to methyl parathion. 

3.2.3.3 Immunological and Lymphoreticular Effects 

A single case report of skin allergy to methyl parathion has been reported in humans (Lisi et al. 1987). 

Also see Section 3.2.3.2. 

No studies were located regarding immunological effects in animals after dermal exposure to methyl 

parathion. 

3.2.3.4 Neurological Effects 

Mental disturbances, manifested as psychiatric sequelae, have been reported after exposure to organophosphates, including methyl parathion. Neuropsychiatric symptoms occurred in two aerial applicators, 

one of whom used methyl parathion as well as other insecticides, including chlorinated insecticides. One 

of these pilots had high levels of exposure to methyl parathion, toxaphene, and Dipterex® with saturation 

of his clothing when the tank of his aircraft accidentally overflowed (Dille and Smith 1964). Several 
METHYL PARATHION 59 

3. HEALTH EFFECTS 

months after the accident, the subject complained of dizziness, anxiety, emotional lability, frequent and 

severe disagreements with family and associates, and inability to perform familiar tasks. 

Erythrocyte cholinesterase levels were monitored in two men exposed dermally to methyl parathion after 

entering a cotton field that had been sprayed with this pesticide (Nemec et al. 1968). The field was 

entered on two separate occasions: twice within 2 hours after an ultra-low-volume spraying and a third 

time within 24 hours after spraying. Dermal methyl parathion residues 2 hours after spraying were 

2–10 mg on the arms; dermal residues 24 hours after spraying were 0.16–0.35 mg on the arms. The 

exposed individuals did not have signs of cholinergic toxicity, but erythrocyte cholinesterase levels after 

the third exposure were 60–65% of preexposure levels. 

Mice that were exposed dermally to residues of methyl parathion in emulsifiable concentrate on foliage, 

and were muzzled to prevent oral intake, developed inhibition of plasma cholinesterase and erythrocyte 

cholinesterase after two 10-hour exposures (Skinner and Kilgore 1982b). For the organophosphate 

pesticides tested in this study, cholinergic signs generally were seen in mice with cholinesterase inhibition 

>50%; results for this end point were not broken down by pesticide. 

In male mice in the dermal LD50 study described under lethality, the ED50 values (doses at which adverse 

effects were observed in 50% of the treated animals) for plasma and red blood cell (RBC) cholinesterase 

inhibition in survivors were 950 and 550 mg/kg, respectively, compared to a dermal LD50 of 1,200 mg/kg 

(Skinner and Kilgore 1982a). The hind feet of the mice were exposed to the pesticide, and the mice were 

muzzled to prevent oral exposure from grooming. Because these ED50 values were obtained in surviving 

mice in a 24-hour LD50 study, they were based on a resistant population, and are not considered suitable 

for inclusion in the LSE tables and figures. 

3.2.3.5 Reproductive Effects 

No studies were located regarding reproductive effects in humans and animals after dermal exposure to 

methyl parathion. 

3.2.3.6 Developmental Effects 

No studies were located regarding developmental effects in humans and animals after dermal exposure to 

methyl parathion. 
METHYL PARATHION 60 

3. HEALTH EFFECTS 

3.2.3.7 Cancer 

No studies were located regarding carcinogenic effects in humans or animals after dermal exposure to 

methyl parathion. 

3.2.4 Other Routes of Exposure 

Ocular effects consisting of electroretinographic changes occurred in mice exposed by the intraperitoneal 

route to an LD50 dose or a dose equal to half of an LD50 dose of methyl parathion (Carricaburu et 

al. 1980). These changes were a direct effect of methyl parathion on repolarization of retinal photoreceptors. Rats, injected intraperitoneally with methyl parathion, developed cholinergic signs at dosage 

levels as low as 1.0 mg/kg/day for 7 days (Hasan and Khan 1985; Khan and Hasan 1988). Exposed rats 

had alterations in brain structural components with an increase in brain lipid, phospholipid, and 

cholesterol content in various portions of the brain (Hasan and Khan 1985) and depletion of gangliosides 

and glycogen (Khan and Hasan 1988). Lipid peroxidation was increased in the cerebrum but inhibited in 

the hindbrain (Hasan and Khan 1985). These changes in brain structural components suggest another 

type of toxic change induced by methyl parathion in the nervous system that could also be responsible for 

some of the acute and chronic neurologic effects seen in humans. Whether such effects could occur in 

humans exposed to low levels of methyl parathion that did not produce overt toxicity is unknown. Assays 

for estrogenic activity of intraperitoneally injected methyl parathion in hemi-ovariectomized rats 

indicated some interference with compensatory ovarian hypertrophy, but a lack of typical estrogenic 

activity (Asmathbanu and Kaliwal 1997; Dhondup and Kaliwal 1997). Fetotoxicity and offspring with 

altered brain enzymes and impaired behavior have been reported in rats after oral or parenteral maternal 

administration of methyl parathion at doses that inhibited acetylcholinesterase activity and, in some 

studies, produced cholinergic signs in the dams (Crowder et al. 1980; Fish 1966; Gupta et al. 1985; 

Tanimura et al. 1967). Pregnant female mice exposed to 60 mg/kg methyl parathion by the 

intraperitoneal route had significantly increased incidences of fetuses with cleft palate and dose-related 

increases in fetal deaths, compared to control litters (Tanimura et al. 1967). Significant increases in 

abnormal sperm morphology were seen in mice following intraperitoneal injection of methyl parathion at 

a dose level of 6 mg/kg (Pagulayan et al. 1994). 
METHYL PARATHION 61 

3. HEALTH EFFECTS 

3.3 GENOTOXICITY 

In a case-control study of pesticide factory workers in Brazil exposed to methyl parathion and formulating 

solvents, the incidence of chromosomal aberrations in lymphocytes was investigated (De Cassia Stocco et 

al. 1982). Though dichlorodiphenyltrichloroethane (DDT) was coformulated with methyl parathion, 

blood DDT levels in the methyl parathion-examined workers and "nonexposed" workers were not 

significantly different. These workers were presumably exposed to methyl parathion via both inhalation 

and dermal routes; however, a dose level was not reported. The exposed workers showed blood 

cholinesterase depressions between 50 and 75%. However, the baseline blood cholinesterase levels in 

nonexposed workers were not reported. No increases in the percentage of lymphocytes with chromosome 

breaks were found in 15 of these workers who were exposed to methyl parathion from 1 week to up to 

7 years as compared with controls. The controls consisted of 13 men who had not been occupationally 

exposed to any chemical and were of comparable age and socioeconomic level. This study is limited 

because of concomitant exposure to formulating solvents, the recent history of exposure for the workers 

was not reported, the selection of the control group was not described adequately, and the sample size was 

limited. 

Chromosome aberrations were detected in lymphocytes of individuals acutely intoxicated by methyl 

parathion by the inhalation route (Van Bao et al. 1974). Blood samples were taken 3–6 days after 

exposure and again at 30 and 380 days. A temporary but significant (p<0.05) increase was noted in the 

frequency of stable chromosomal aberrations in the exposed individuals. The study limitations include 

small sample size, absence of a control group, lack of quantification of exposure levels, and a possible 

concomitant exposure to other substances via the dermal route. 

No studies were located regarding genotoxic effects in animals after inhalation exposure to methyl 

parathion. 

The lymphocytes from 31 patients exposed to various organophosphate pesticides were examined for 

chromosomal aberrations (Van Bao et al. 1974). Five of the patients were exposed to methyl parathion 

only. Blood samples were taken 3–6 days after exposure and again at 30 and 180 days. A significant 

(p<0.05) increase was noted in the frequency of stable chromosomal aberrations in acutely intoxicated 

persons (although such cells are eventually lost from the cell population). Two of the methyl parathionexposed persons had taken large doses orally in suicide attempts. The study limitations include small 

sample size, absence of a control group, lack of quantification of exposure levels, and possible 
METHYL PARATHION 62 

3. HEALTH EFFECTS 

concomitant exposure to other substances via the dermal route. Although the study did not quantify the 

exposure levels, the results suggest that methyl parathion can exert direct genotoxic effects on 

chromosomes. 

In a similar study, the lymphocytes from five patients who ingested methyl parathion (Wofatox) in 

suicide attempts were examined for aneuploidy, chromatid aberrations, and chromosome aberrations 

(Czeizel 1994). No significant differences from the 15 control patients were seen in these end points. 

The controls were patients who had undergone appendicitis or hernia surgery, and were matched for sex, 

age, and socioeconomic status with a larger set of 31 pesticide poisoning cases, of which the methyl 

parathion cases were a subset. Limitations of this study include the small number of methyl parathion 

cases, and the use of appendicitis and other surgery patients as controls. 

Methyl parathion administered to male mice in the diet or drinking water did not increase the incidence of 

resorption of fetuses in mated dams (Degraeve et al. 1985; Waters et al. 1982). In mice, dietary exposure 

to the maximum tolerated dose, and one-half and one-quarter of the maximum tolerated doses failed to 

produce preimplantation embryo loss from the resultant matings with untreated females (Waters et 

al. 1982). However, no specific details regarding the actual doses administered were provided by the 

authors. The findings of these two studies were also supported by the absence of a dominant-lethal effect 

in mice receiving 0.026 mg/kg/day of methyl parathion in drinking water for 7 weeks (Degraeve et 

al. 1984a). This result suggests that methyl parathion is not toxic to male mouse germ cells. However, 

relatively high levels of methyl parathion can result in changes in sperm morphology. Male mice, orally 

exposed (gavage) to doses in the range of 9.375–75 mg/kg, exhibited dose-related significantly increased 

percentages of abnormal sperm at all doses (Mathew et al. 1992). Significant increases in abnormal 

sperm morphology were also seen in mice following intraperitoneal injection of 6 mg /kg, but not 

1.3 mg/kg (Pagulayan et al. 1994). Of two studies in Drosophila melanogaster, one (Tripathy et al. 1987) 

showed mutagenic effects in somatic and germ cell lines and induction of sex-linked recessive lethals, 

whereas the other one (Waters et al. 1982) provided negative results. 

Methyl parathion has been tested in numerous genotoxicity assays using prokaryotic and eukaryotic 

systems with both positive and negative results. Results of these studies are summarized in Tables 3-5 

and 3-6. 

When methyl parathion was tested in Salmonella typhimurium, contradictory results were reported with 

or without using metabolic activation (Rashid and Mumma 1984; Shigaeva and Savitskaya 1981; Waters 
Table 3-5. Genotoxicity of Methyl Parathion In Vivo 

Species (test system) End point Results Reference Eukaryotic organisms: 

Drosophila melanogaster/males Recessive lethal – Waters et al. 1982 

D. melanogaster/dietary exposure Recessive lethal somatic + Tripathy et al. 198

mutation

Mammalian cells: 

Rat bone marrow/intraperitoneal injection Induction of micronuclei + Grover and Malhi 

Mouse/oral exposure; diet or drinking water Dominant lethal – Degraeve et al. 19

Mouse/oral exposure; drinking water Chromosomal aberrations – Degraeve et al. 19

Mouse/intraperitoneal administration Chromosomal aberrations – Huang 1973 Mouse/oral exposure; gavage Sperm shape abnormalities + Mathew et al. 1992 Human lymphocytes/dermal and inhalation exposure Chromosomal aberrations – De Cassia Stocco Human lymphocytes/oral exposure Chromosomal aberrations + Van Bao et al. 197Human lymphocytes/oral exposure Chromosomal aberrations – Czeizel 1994 

– = negative result; + = positive result; (+) = weakly positive result 
Table 3-6. Genotoxicity of Methyl Parathion In Vitro 

Results 

Species (test system) End point 

With activation 

Without activation Reference 

Prokaryotic organisms: 

Bacteria: 

Salmonella typhimurium/plate incorporation 

Reverse mutation – 

+ 

– 

– 

Waters et al. 1982 

Rashid and Mumm

No data + Shigaeva and Savi

Escherichia coli/WP2;plate incorporation Reverse mutation – – Dean 1972; Waters E. coli/K-12 COIE/plasmid DNA DNA damage No data + Griffin and Hill 197

E. coli/plate incorporation 5-Methyltryptophan resistance No data + Mohn 1973 

Eukaryotic organisms: 

Yeast: 

Saccharomyces cerevisiae (D7)/plate incorporation 

Reverse mutation – – Waters et al. 1982 

S. cerevisiae (D3)/plate incorporation Mitotic recombination No data + Waters et al. 1982 

S. cerevisiae (D7)/spot test Gene conversion – – Waters et al. 1982 

S. typhimurium DNA damage No data + Rashid and Mumm

Mammalian cells: 

Chinese hamster ovary Sister chromatid exchange + – Waters et al. 1982 

Chinese hamster V79 Sister chromatid exchange No data + Chen et al. 1981 

Human lymphoid cells/LAZ-007 Sister chromatid exchange No data + Sobti et al. 1982 

Human lymphocytes Sister chromatid exchange No data + Chen et al. 1981; G

1987 

Burkitt lymphoma/835M Sister chromatid exchange No data + Chen et al. 1981 

Human lymphocytes Chromosomal aberrations No data + Kumar et al. 1993 
Table 3-6. Genotoxicity of Methyl Parathion In Vitro (continued) 

Results 

With Without 

Species (test system) End point activation activation Reference 

Human hematopoietic cells/RPMI 1788, Chromosomal damage No data – Degraeve et al. 1987191; B411-4 Human lung fibroblasts Unscheduled DNA synthesis – – Waters et al. 1982 

– = negative result; + = positive result; DNA = deoxyribonucleic acid 
METHYL PARATHION 66 

3. HEALTH EFFECTS 

et al. 1982). However, it tested negative in Saccharomyces cerevisiae strain D7 for both reverse mutation 

and gene conversion (Waters et al. 1982) and in Escherichia coli WP 2 for reverse mutation (Dean 1972). 

Methyl parathion treatment resulted in a negative response for reverse mutation (Waters et al. 1982) but a 

positive response for 5-methyl tryptophan resistance assay (Mohn 1973) in E. coli. Positive results were 

also reported for mitotic recombination in S. cerevisiae D3 (Waters et al. 1982) and for deoxyribonucleic 

acid (DNA) damage in S. typhimurium (Rashid and Mumma 1984) and E. coli (Griffin and Hill 1978). 

Methyl parathion gave a negative response for unscheduled DNA synthesis in cultured human lung 

fibroblasts (Waters et al. 1982). 

Results of methyl parathion assays involving effects on chromosomes have also been contradictory. For 

sister chromatid exchange, Waters et al. (1982) reported a positive response in Chinese hamster ovary 

cells only in the presence of metabolic activation system, while methyl parathion tested positive without a 

metabolic activation system in Chinese hamster V79 cells (Chen et al. 1981), cultured normal human 

lymphoid cells (Chen et al. 1981; Gomez-Arroyo et al. 1987; Sobti et al. 1982), and Burkitt's lymphoma 

cells (Chen et al. 1981). Chen et al. (1981) found a significant dose-related increase in sister chromatid 

exchange in both hamster and human cultured cells, but dose-related cell cycle delays were less 

pronounced in human cell lines than in V79 cells. Negative results were obtained for chromosomal 

aberrations in human lymphocytes without a metabolic activation system (Kumar et al. 1993). 

Induction of micronuclei has been reported in bone marrow cells of rats injected intraperitoneally with 

methyl parathion (Grover and Malhi 1985). Although negative results were obtained for chromosomal 

aberrations in mouse cells and human hematopoietic cells (Degraeve et al. 1984a; Huang 1973), 

contradictory results were reported in human lymphocytes following exposure of humans to methyl 

parathion (Czeizel 1994; De Cassia Stocco et al. 1982; Van Bao et al. 1974). Exposure to other 

compounds complicates interpretation. In the dominant lethal assay, no increase in the incidence of preor postimplantation fetal lethality was found in the litters of male mice following oral exposure (Degraeve 

et al. 1985; Jorgensen et al. 1976; Waters et al. 1982), but an assay for sperm shape abnormalities yielded 

positive results at relative high oral doses (Mathew et al. 1992). Thus, the available evidence is 

inconclusive, and no determination regarding the potential genotoxic risks of methyl parathion exposure 

for humans can be made. 
METHYL PARATHION 67 

3. HEALTH EFFECTS 

3.4 TOXICOKINETICS 

Methyl parathion can be readily absorbed by humans following inhalation, oral, or dermal exposure, 

although quantitative data are lacking. Studies in animals indicate that oral absorption following single 

doses can amount to 80% of the administered dose within a few days of dosing. A single dermal study in 

rats also suggested almost complete absorption of an applied dose within a 96-hour period. No data are 

available regarding pulmonary absorption of methyl parathion in animals. Methyl parathion was found to 

be widely distributed in organs and tissues of rats following dermal exposure, but first-pass metabolism 

greatly limits its distribution following oral absorption. Methyl parathion has been detected in human 

breast milk and studies in animals have shown that it can cross the placenta and be transferred to the fetus. 

Methyl parathion is rapidly and extensively metabolized, mainly in the liver, to polar substances that are 

quickly excreted in the urine. Oxidative desulfuration by microsomal oxidases transforms methyl 

parathion into the neurotoxic, active metabolite, methyl paraoxon; the specific isozyme involved in this 

reaction has not been identified. Other reactions including oxidation, hydrolysis, dearylation, and 

dealkylation detoxify methyl parathion. A major detoxification pathway is enzymatic hydrolysis of 

methyl paraoxon to dimethyl phosphate and 4-nitrophenol. These metabolites are eliminated primarily in 

the urine in humans, rats, and mice. 

3.4.1 Absorption 

Often, absorption occurs by multiple routes in humans. Dean et al. (1984) reported deaths and toxic 

effects as well as lowered blood cholinesterase levels and excretion of urinary 4-nitrophenol in several 

children who were exposed by inhalation, oral, and possibly dermal routes after the spraying of methyl 

parathion in a house. In the same incident (Dean et al. 1984), absorption was indicated in adults who also 

excreted 4-nitrophenol in the urine, though at lower levels than some of the children, and in the absence 

of other evidence of methyl parathion exposure. In this study, the potential for age-related differences in 

absorption rates could not be assessed because exposure levels were not known and the children may have 

been more highly exposed than the adults. Health effects from multiple routes are discussed in detail in 

Section 3.2. 

3.4.1.1 Inhalation Exposure 

No studies were located regarding absorption in humans and animals after inhalation exposure to methyl 

parathion. However, it can be concluded that pulmonary absorption occurred in humans as evidenced by 
METHYL PARATHION 68 

3. HEALTH EFFECTS 

toxic systemic effects found in humans dying after acute inhalation exposure to methyl parathion 

(Fazekas 1971). 

3.4.1.2 Oral Exposure 

Absorption following acute oral exposure is indicated in a study in which four volunteers received methyl 

parathion once a day with food for 5 consecutive days (Morgan et al. 1977). Urine was collected for 

24 hours after each dose and for 2 days after the last dosing day. The average 24-hour excretions of the 

metabolites 4-nitrophenol and dimethyl phosphate following each dose accounted for 27 and 12% of the 

ingested dose, respectively. The highest rate of excretion for 4-nitrophenol occurred during the first 

4 hours after dosing, and for dimethyl phosphate, occurred during in the interval from 4 to 8 hours after 

dosing. These results indicate rapid absorption. 

Rapid and efficient absorption in animals follows oral administration of methyl parathion (Braeckman et 

al. 1983; Hollingworth et al. 1967). Oral absorption was 77 and 79% in two dogs receiving 3 mg/kg of 

35S-labeled methyl parathion by gavage (Braeckman et al. 1983). This conclusion was based on a 

comparison of the 6-day urinary excretion of radioactivity after gavage administration versus intravenous 

injection. In mice, 80% of the radioactivity from a gavage dose of 3 mg/kg of 32P-labelled methyl 

parathion was recovered as radiolabeled metabolites in the urine, and up to 10% was recovered in the 

feces at 72 hours (Hollingworth et al. 1967). Estimates of fecal excretion were considered unreliable. 

Therefore, based on 80% recovery in the urine, it can be concluded that at least 80% of the dose was 

absorbed following oral administration of methyl parathion. Approximately 75% of the urinary excretion 

occurred within the first 12 hours. Furthermore, decreased cholinesterase activity (Ceron et al. 1995; 

Miyamoto et al. 1963b) and detection of methyl parathion urinary metabolites (Chang et al. 1997; 

Youssef et al. 1987) after oral doses of methyl parathion provide indirect evidence of absorption in 

animals. 

The data presented above suggest that methyl parathion would be absorbed by humans following 

ingestion of food and drinking water contaminated with methyl parathion. However, no data are available 

on the rate and extent of absorption in humans. 
METHYL PARATHION 69 

3. HEALTH EFFECTS 

3.4.1.3 Dermal Exposure 

Epidemiological studies indicate that absorption of methyl parathion occurs in humans following acute 

dermal exposure (Nemec et al. 1968; Ware et al. 1973, 1974, 1975). On two separate occasions, two 

entomologists were in a field for 5 minutes, 2 hours after it was sprayed with methyl parathion; 2–10 mg 

methyl parathion was measured on the skin of both arms (Nemec et al. 1968). A third exposure occurred 

24 hours after spraying the field; levels of methyl parathion on the skin of the arms ranged from 0.163 to 

0.351 mg methyl parathion. Blood cholinesterase levels after the three exposures were 60% of preexposure levels in these subjects, which suggests that absorption had occurred (Nemec et al. 1968). Two 

volunteers entered treated cotton fields for 30-minute periods at 0, 12, 24, 48, and 72 hours postexposure 

(Ware et al. 1973). Twenty-four hours after exposure, 0.027 and 0.032 mg/L methyl parathion were 

detected in the serum. The skin was considered to be the major route of exposure in this study (Ware et 

al. 1973). In five subjects, the amount of methyl parathion on the hands averaged 1.7 mg following 

5 hours of exposure in fields that had been sprayed with methyl parathion 12 hours earlier (Ware et al. 

1975). The amount of methyl parathion averaged 2.2 mg on the arms, 0.4 mg on the torso, 0.03 mg on 

the legs, 10.6 mg on the shirts, and 40.0 mg on the pants. The serum contained 70–227 ppb of methyl 

parathion 3–7 hours after the 5-hour exposure compared with 0–4 ppb at 24 hours. Serum levels were 

highest immediately after exposure (0.156 mg/L); after 48 hours, cumulative levels of urinary 4-nitrophenol varied between 1.1–23 mg. 

Although the extent of absorption was not measured, the above evidence suggests that absorption in 

humans occurs rapidly following dermal exposure to commercial pesticide formulations of methyl 

parathion. 

In a study of pregnant rats exposed to 10 mg/kg of radiolabeled methyl parathion (in acetone) that was 

applied to the back of the neck (unoccluded), approximately half of the dose was absorbed within 1 hour 

postapplication, and 95% was absorbed within 96 hours. Skin disappearance rate constants of 0.35 hour-1 

and 0.03 hour-1 were estimated, and corresponded to half-lives of 2 and 22 hours, respectively (AbuQuare et al. 2000). Although animals were housed individually, the possibility of some degree of oral 

absorption could not be discounted. Additional evidence of dermal absorption comes from the finding of 

inhibition of plasma cholinesterase activity in mice following dermal exposure to methyl parathion 

(Skinner and Kilgore 1982b). 
METHYL PARATHION 70 

3. HEALTH EFFECTS 

3.4.2 Distribution 

3.4.2.1 Inhalation Exposure 

No studies were located regarding distribution in humans or animals after inhalation exposure to methyl 

parathion. Although cases of inhalation exposure have been reported, there were no data that provided 

detailed information on the distribution of methyl parathion residues in various tissues. 

3.4.2.2 Oral Exposure 

No studies were located regarding distribution in humans after oral exposure to methyl parathion. 

Following a single gavage administration of 20 mg/kg methyl parathion, the highest serum concentration 

reported in dogs ranged from 0.13 to 0.96 μg/mL 3–9 hours postexposure (Braeckman et al. 1983). The 

low systemic availability of methyl parathion following oral gavage in dogs was suggested to be the result 

of hepatic first-pass metabolism (Braeckman et al. 1983). 

Placental transfer of methyl parathion was demonstrated following oral administration to pregnant rats 

1–3 days before parturition (Ackermann and Engst 1970). Thirty minutes after administration, methyl 

parathion was found in fetal brain, liver, and muscle, and in the placenta and maternal liver, suggesting its 

rapid distribution. The fetal liver concentration of methyl parathion was nearly 2-fold that of the maternal 

liver and approximately half of the concentration found in the placenta. Small amounts of methyl 

paraoxon, the oxidative metabolite of methyl parathion, were found in fetal brain, liver, and muscle, but 

could not be detected in maternal liver or placental tissue. Although the source of exposure was not 

determined, methyl parathion was detected in breast milk of 8/90 women tested in 5 of 10 regions of 

central Asia (Lederman 1996). Methyl parathion was not detected in the breast milk of mothers tested in 

the other 5 regions (Lederman 1996) or in breast milk of 11 Italians tested for the presence of a number of 

pesticides, including methyl parathion (Roggi et al. 1991). A study of a mixture of pesticides (methyl 

parathion, lindane, and permethrin) in rats reported that methyl parathion was present in higher 

concentrations in the dams’ milk and in the pups’ blood than in the dams’ blood following oral exposure 

of the dams on lactation days 1–14 (Golubchikov 1991; Goncharuk et al. 1990). Confidence in these 

findings is low because descriptions of the methods and results were cursory. 
METHYL PARATHION 71 

3. HEALTH EFFECTS 

The available data are insufficient to determine the pattern or extent of distribution in human tissues after 

oral exposure to this compound. 

3.4.2.3 Dermal Exposure 

There is limited information available regarding the distribution of methyl parathion after dermal 

exposure in humans. Two subjects, dermally exposed to methyl parathion, had 2.74 and 1.23 mg on their 

hands. Twenty-four hours after exposure, the serum levels were 0.027 and 0.032 mg/L, respectively 

(Ware et al. 1973). Twelve hours after cotton fields were sprayed, five men entered the treated fields for 

5 hours. An average of 1.7 mg methyl parathion was detected on their hands. Serum concentrations 

averaged 0.156 mg/L in these subjects after 3 hours of exposure. Levels decreased to 0.1 and 0.002 mg/L 

at 2 and 24 hours postexposure, respectively (Ware et al. 1975). Although 0.5 mg methyl parathion was 

detected on the hands of four subjects, none was found in the serum (Ware et al. 1974). No information 

on the tissue distribution of methyl parathion in humans was found. 

Following single dermal applications of 10 mg/kg of radiolabeled methyl parathion to pregnant rats, 

methyl parathion was found to be widely distributed to all major tissues and organs. Concentrations were 

highest in plasma and kidney, maximum levels measured 2 hours postapplication. Peak levels in liver, 

brain, fetus, and placenta, were measured 2 to 10 hours later, at which times the highest concentration of 

methyl parathion was in the fetus (Abu-Quare et al. 2000). 

3.4.2.4 Other Routes of Exposure 

Distribution of methyl parathion was rapid when it was administered intravenously to rats (3 and 

15 mg/kg) and guinea pigs (20 and 40 mg/kg) (Miyamoto 1964). Levels were highest in the brain, liver, 

lungs, kidneys, and heart of these animals at 2.5 minutes postexposure (Miyamoto 1964). The levels of a 

metabolite, methyl paraoxon, were highest in the lungs and liver of guinea pigs, and in the liver of rats. 

However, it should be noted that the protein-bound oxygen analog was not measured in the study. Serum 

methyl parathion levels were highest in dogs immediately following intravenous exposure (Braeckman et 

al. 1980). The serum concentrations declined rapidly, followed by a slower clearance, beginning at 

5 hours postexposure, for doses of 3, 10, or 30 mg/kg methyl parathion. Intraperitoneal injection of 

methyl parathion in pregnant rats has resulted in fetal toxicity, expressed in reduced fetal brain 

cholinesterase levels; this is another indication that methyl parathion and/or its toxic metabolite can cross 

the placental barrier (Fish 1966). 
METHYL PARATHION 72 

3. HEALTH EFFECTS 

The protein binding of methyl parathion in vitro was 93% in dog serum and 94% in human serum 

(Braeckman et al. 1983). The protein binding of methyl parathion in a solution of human albumin that 

approximated the concentration of albumin in human serum also was 94%, suggesting that albumin is the 

main binding protein for methyl parathion in serum. Albumin probably acts as a transport protein, 

because although the degree of protein binding in serum is high, a high volume of distribution has been 

determined for methyl parathion in the dog (Braeckman et al. 1980, 1983). 

3.4.3 Metabolism 

Methyl parathion is a phosphorothioate, which refers to the organophosphate compounds that contain the 

P=S substructure (Nakatsugawa et al. 1968). The metabolism of methyl parathion has been well studied 

in vitro using rat, mouse, rabbit, guinea pig, and human liver homogenates (Benke and Murphy 1975; 

Hollingworth et al. 1973; Nakatsugawa et al. 1968; Neal and DuBois 1965) and in situ using intact rat 

livers (Zhang and Sultatos 1991). Metabolism has also been studied in vivo using pregnant rats exposed 

by dermal application of radiolabeled methyl parathion (Abu-Qare et al. 2000). No metabolism studies 

were conducted by the inhalation route. The low systemic availability of methyl parathion after oral 

administration in dogs, and the high hepatic extraction ratios after intravenous administration, suggest 

first-pass metabolism by the liver (Braeckman et al. 1983). The proposed metabolic pathway based on 

the results of in vitro studies is shown in Figure 3-3 (Benke and Murphy 1975). This compound can be 

activated (oxidative desulfuration) to its toxic metabolite, methyl paraoxon, in vitro using mouse liver 

homogenates (Benke et al. 1974) and in situ (Zhang and Sultatos 1991) in rats (see reaction 1 in 

Figure 3-3). Methyl paraoxon has been found in liver and brain of rats following dermal exposure to 

methyl parathion (Abu-Qare et al. 2000). This intermediate oxygen analog is more potent than the parent 

compound in inhibiting cholinesterase enzyme activity and causing the neurotoxic effects of methyl 

parathion (Benke et al. 1974). This oxidative reaction requires microsomal oxidases, NADPH, and 

oxygen (Benke et al. 1974; Hollingworth et al. 1973; Nakatsugawa et al. 1968). 

The detoxification of methyl parathion may occur through any of several metabolic processes (i.e., 

oxidation, hydrolysis, dearylation, and dealkylation) (Benke and Murphy 1975; Benke et al. 1974; 

Hollingworth et al. 1973; Nakatsugawa et al. 1968; Neal and DuBois 1965). A major detoxification 

pathway is enzymatic hydrolysis of the toxic metabolite, methyl paraoxon to dimethyl phosphate and 

4-nitrophenol (reaction 3 in Figure 3-3) (Benke and Murphy 1975; Benke et al. 1974). In humans, rats, 

and mice, these nontoxic metabolites are eliminated primarily in the urine (Hollingworth et al. 1973; 

Morgan et al. 1977; Plapp and Casida 1958). Another detoxifying pathway (reaction 2) is the oxidation 
Figure 3-3. Proposed Metabolic Pathways of Methyl Parathion 

CH3O S GSH = Glutathione 

Ar = p-Nitrophenyl + GS Ar 

OH CH3O 

Dimethyl thiophosphate 

P 

Dearylation 6. GSH 

CH S Dealkylation CH3O S Oxidation CH3O S 3O 

2. 4. P P P + HO 

GS R + 

GSH NADPH, 

O 2 4-N

O OH 

Dimethyl thiophosphate 

O Ar CH3O O Ar CH3O 

Desmethyl methyl parathion Methyl parathion 

NADPH, 1. 

O 2

CH O Dealkylation 3O O Hydrolysis CH3O 

O CH3O 

5. 3. P GS R + P + HO 

P GSH 

H2O, Ca++ 4-N

HO O Ar OH CH3O O Ar CH3O O-Methyl-O-4-nitrophenyl Dimethyl phosphate phosphate Methyl paraoxon 

Dearylation 7. 

GSH 

Bound to Nonvital CH3O O Acetylcholinesterase Tissue Sites Inhibition 

P + GS Ar 

CH3O OH

*Adapted from Benke and Murphy (1975) Dimethyl phosphate 

The numbered reactions (1-7) are reference numbers for pathways discussed in the text. 
METHYL PARATHION 74 

3. HEALTH EFFECTS 

of the aryl group in the parent compound to produce dimethyl thiophosphate and 4-nitrophenol. The 

reaction occurs only in the presence of NADPH (Nakatsugawa et al. 1968) and has been studied in liver 

homogenates of rats, rabbits, mice, and guinea pigs (Benke et al. 1974; Nakatsugawa et al. 1968; Neal and 

Dubois 1965). Radiolabeled 4-nitrophenol has been detected in the liver of rats following dermal 

exposure to radiolabeled methyl parathion (Abu-Qare et al. 2000). Dimethyl thiophosphate has been 

detected in the urine of rats treated with methyl parathion (Plapp and Casida 1958). The 4-nitrophenol 

can be glucuronidated to form 4-nitrophenol glucuronide (Zhang and Sultatos 1991). 

In vitro studies indicate that detoxification of methyl parathion and methyl paraoxon can occur by 

glutathione-dependent alkyltransferase and aryltransferase (Benke and Murphy 1975; Benke et al. 1974). 

Glutathione (GSH) alkyltransferase converts methyl parathion to desmethyl methyl parathion (reaction 4 

in Figure 3-3), and methyl paraoxon to O-methyl-O-4-nitrophenol phosphate (reaction 5 in Figure 3-3). 

Glutathione aryltransferase produces dimethyl thiophosphate from methyl parathion (reaction 6 in 

Figure 3-3), and dimethyl phosphate from methyl paraoxon (reaction 7 in Figure 3-3) (Benke and Murphy 

1975). The addition of glutathione in liver homogenates increases the disappearance of methyl parathion 

and methyl paraoxon in mice (Benke et al. 1974). Pretreatment with dimethyl maleate, which reduces 

glutathione levels, potentiated toxicity in mice (Mirer et al. 1977), but not in female rats (Chambers et al. 

1994). Zhang and Sultatos (1991) did not detect methyl parathion-related glutathione conjugates in the 

effluent or bile of rat livers perfused in situ with 20–80 μM solutions of methyl parathion. Although the 

Mirer et al. (1977) study indicates that glutathione conjugation might be involved in detoxification of 

methyl parathion in mice, it should be noted that near lethal concentrations of methyl parathion were used 

in the intraperitoneal studies, and in vitro studies employed exposure levels higher than those likely to be 

encountered in sublethal in vivo toxicity studies. Glutathione-dependent metabolism of methyl parathion, 

therefore, may not be a significant detoxification pathway in vivo at sublethal toxic concentrations in 

which access to glutathione S-transferases might be concentration limited (Huang and Sultatos 1993). 

Methyl paraoxon may also be made unavailable by binding to noncritical tissue and plasma constituents 

(Benke and Murphy 1975), including cholinesterase (Parkinson 1996). In addition, the parent compound 

is bound to albumin, in serum, as discussed previously in Section 3.4.2.4, but this binding does not appear 

to limit the availability of methyl parathion to the tissues, indicating that it is reversible. Tissue binding 

appears to be more important than serum binding (Braeckman et al. 1980, 1983). 

The relative rates of activation and detoxification of methyl paraoxon within the liver determine whether 

net activation or detoxification will occur (Sultatos 1987). Sex-differences have been observed in acute 
METHYL PARATHION 75 

3. HEALTH EFFECTS 

LD50 values for methyl parathion (see Section 3.2.2.1). The lower LD50 values in male (compared to 

female) rats may possibly be attributed to enhanced activation of thio-organophosphate pesticides in the 

liver of male rats as reported by Murphy and DuBois (1958). Acute intraperitoneal LD50 values in male 

and female rats increase with increasing postpartum age, up to approximately 35–40 days for males and 

60 days for females (Benke and Murphy 1975). It has also been found that the metabolism of methyl 

parathion is affected by the age of rats (Benke and Murphy 1975). The age-related ratios of oxidative 

deactivation (reaction 2 in Figure 3-3) to oxidative activation (reaction 1) of methyl parathion correlated 

with the LD50 values better than did either measure alone. In addition, age-related increases in hydrolysis 

(reaction 3), glutathione-dependent dealkylation and dearylation (reactions 5 and 7), and tissue binding of 

methyl paraoxon correlated with the increase in LD50 values (Benke and Murphy 1975), indicating that 

detoxification pathways for methyl parathion may be more effective in 60-day-old rats than in younger 

ones (Benke and Murphy 1975). However, at present, mechanisms relating to increased susceptibility of 

immature rats relative to adults are not fully understood. 

3.4.4 Elimination and Excretion 

4-Nitrophenol and 4-nitrophenol glucuronide are excreted in urine. The studies of urinary excretion of 

methyl parathion metabolites, including those reported in this section, generally hydrolyze the 

glucuronide prior to analysis and report the resulting total 4-nitrophenol values. 

3.4.4.1 Inhalation Exposure 

Most of the toxic effects caused by methyl parathion resulted from exposure by multiple routes, 

especially for workers in sprayed fields or formulating facilities, or people in homes. Dean et al. (1984) 

reported deaths and toxic effects in several children as well as lowered blood cholinesterase levels and 

excretion of urinary 4-nitrophenol (adults showing no adverse effects also excreted 4-nitrophenol). 

Health effects from multiple routes have been discussed in detail in Section 3.2. 

No studies were located regarding excretion in animals after inhalation exposure to methyl parathion. 

3.4.4.2 Oral Exposure 

Limited information was available regarding excretion in humans after oral exposure to methyl parathion. 

During 5 days of exposure of four subjects to 2 or 4 mg of methyl parathion once daily in food (0.028 or 
METHYL PARATHION 76 

3. HEALTH EFFECTS 

0.057 mg/kg/day), the average 24-hour excretions of the metabolites dimethyl phosphate and 4-nitrophenol accounted for 27 and 12% of the administered dose, respectively (Morgan et al. 1977). An 

average of 60 and 86% of the total urinary excretion of 4-nitrophenol had been eliminated at 4 and 

8 hours, respectively, after ingestion of each dose. Thus, the highest recoveries of 4-nitrophenol occurred 

during the first 4 hours after exposure. Dimethyl phosphate was excreted mainly during the interval from 

4 to 8 hours after exposure (Morgan et al. 1977). However, there was a low and variable recovery of 

alkyl phosphate metabolites from spiked urine samples (Morgan et al. 1977). Nevertheless, the available 

data suggest that methyl parathion metabolites are rapidly excreted in humans following oral exposure. 

Urinary excretion of metabolites of methyl parathion is rapid and efficient in animals (Braeckman et al. 

1983; Hollingworth et al. 1967). In mice, 70–80% of the 32P activity was excreted in the urine within 

72 hours after an acute exposure to radiolabeled methyl parathion (Hollingworth et al. 1967). Excretion 

in the feces represented, at most, 10% of the total radioactivity recovered. Dimethyl phosphate was the 

major metabolite in mice (Hollingworth et al. 1973). At 24 hours, urinary excretion of dimethyl 

phosphate was 53 and 31.9% of the activity for 3- and 17-mg/kg doses, respectively (Hollingworth et al. 

1973). In rats, urinary dimethyl thiophosphate accounted for 27% of the dose of radioactivity from 

2 mg/kg of methyl parathion 24 hours after oral administration. In two dogs, the cumulative radioactivity 

in the urine 6 days after exposure was 63 and 78% of the 3 mg/kg oral dose (Braeckman et al. 1983). 

Single oral (gavage) doses of 1.4–7.0 mg methyl parathion/kg, administered to rats, were followed by 

24-hour excretion of 2.8–22.0 μg 4-nitrophenol/mL urine with a linear correlation (Chang et al. 1997). 

The available evidence suggests that excretion of methyl parathion metabolites in humans and animals 

following acute oral exposure is essentially the same and occurs rapidly. Excretion occurs primarily via 

the urine. Methyl parathion can also be excreted in breast milk, although it has been detected only in a 

limited number of samples from women of central Asia, for which exposure data were not available 

(Lederman 1996) (see also Section 3.4.2.2). A study in rats also reported excretion of methyl parathion in 

the milk (Golubchikov 1991; Goncharuk et al. 1990). 

3.4.4.3 Dermal Exposure 

Only two studies were available that reported detection of a metabolite of methyl parathion in the urine of 

persons dermally exposed to methyl parathion (Ware et al. 1974, 1975). Four subjects were exposed for 

5 hours to a methyl parathion formulation in a field that had been sprayed 24 hours prior to exposure 

(Ware et al. 1974). At 48 hours, an average of 0.5 mg 4-nitrophenol was found in the urine, but 
METHYL PARATHION 77 

3. HEALTH EFFECTS 

4-nitrophenol recoveries were low and variable. In a later study using a different analytical method, an 

average of 1.98 mg 4-nitrophenol was measured in the urine of five men exposed for 5 hours (Ware et al. 

1975). The absorption, distribution, and excretion of methyl parathion were evident from these studies. 

Air levels in the Ware et al. (1975) study averaged 12.6 ng/m3

, with an average respiratory dose of 75 ng 

for the 5-hour exposure. Dislodgeable residues on the skin just after spraying (at a level of 1 lb active 

ingredient/acre) ranged from 3.5 to 24 mg, and after 12 hours, they were 2.1–16 mg. 

In a study of pregnant rats that were exposed to radiolabeled methyl parathion by single dermal 

application, half-life elimination rate constants for various tissues ranged from 0.04 to 0.07 hour-1, highest 

values noted in plasma, kidneys, and fetus. Of the applied radioactivity, 14% was recovered in the urine 

in the first hour postapplication. By the end of the 96-hour study, 91% of the applied dose had been 

recovered in the urine. Fecal excretion accounted for only 3% of the administered dose (Abu-Qare et al. 

2000). 

3.4.4.4 Other Routes of Exposure 

The elimination of methyl parathion following intravenous injection is rapid in dogs (Braeckman et al. 

1980, 1983). Two dogs received 3 mg/kg 35S-methyl parathion intravenously. Urinary excretion was 

80–96% of the dose of radioactivity within the 6 hours following injection. Measurement of plasma 

concentrations of radioactivity before and after passage through the liver indicated high hepatic extraction 

(Braeckman et al. 1983). Thus, similar elimination data were obtained for both the intravenous and oral 

routes of exposure. The mean terminal half-life for elimination of a 10-mg/kg intravenous dose of methyl 

parathion was determined through modeling of the data to be 7.2 hours (Braeckman et al. 1980). 

3.4.5 Physiologically Based Pharmacokinetic (PBPK)/Pharmacodynamic (PD) Models 

Physiologically based pharmacokinetic (PBPK) models use mathematical descriptions of the uptake and 

disposition of chemical substances to quantitatively describe the relationships among critical biological 

processes (Krishnan et al. 1994). PBPK models are also called biologically based tissue dosimetry 

models. PBPK models are increasingly used in risk assessments, primarily to predict the concentration of 

potentially toxic moieties of a chemical that will be delivered to any given target tissue following various 

combinations of route, dose level, and test species (Clewell and Andersen 1985). Physiologically based 

pharmacodynamic (PBPD) models use mathematical descriptions of the dose-response function to 

quantitatively describe the relationship between target tissue dose and toxic end points. 
METHYL PARATHION 78 

3. HEALTH EFFECTS 

PBPK/PD models refine our understanding of complex quantitative dose behaviors by helping to 

delineate and characterize the relationships between: (1) the external/exposure concentration and target 

tissue dose of the toxic moiety, and (2) the target tissue dose and observed responses (Andersen et al. 

1987; Andersen and Krishnan 1994). These models are biologically and mechanistically based and can 

be used to extrapolate the pharmacokinetic behavior of chemical substances from high to low dose, from 

route to route, between species, and between subpopulations within a species. The biological basis of 

PBPK models results in more meaningful extrapolations than those generated with the more conventional 

use of uncertainty factors. 

The PBPK model for a chemical substance is developed in four interconnected steps: (1) model 

representation, (2) model parametrization, (3) model simulation, and (4) model validation (Krishnan and 

Andersen 1994). In the early 1990s, validated PBPK models were developed for a number of 

toxicologically important chemical substances, both volatile and nonvolatile (Krishnan and Andersen 

1994; Leung 1993). PBPK models for a particular substance require estimates of the chemical substancespecific physicochemical parameters, and species-specific physiological and biological parameters. The 

numerical estimates of these model parameters are incorporated within a set of differential and algebraic 

equations that describe the pharmacokinetic processes. Solving these differential and algebraic equations 

provides the predictions of tissue dose. Computers then provide process simulations based on these 

solutions. 

The structure and mathematical expressions used in PBPK models significantly simplify the true 

complexities of biological systems. If the uptake and disposition of the chemical substance(s) is 

adequately described, however, this simplification is desirable because data are often unavailable for 

many biological processes. A simplified scheme reduces the magnitude of cumulative uncertainty. The 

adequacy of the model is, therefore, of great importance, and model validation is essential to the use of 

PBPK models in risk assessment. 

PBPK models improve the pharmacokinetic extrapolations used in risk assessments that identify the 

maximal (i.e., the safe) levels for human exposure to chemical substances (Andersen and Krishnan 1994). 

PBPK models provide a scientifically sound means to predict the target tissue dose of chemicals in 

humans who are exposed to environmental levels (for example, levels that might occur at hazardous waste 

sites) based on the results of studies where doses were higher or were administered in different species. 

Figure 3-4 shows a conceptualized representation of a PBPK model. 
3. HEALTH EFFECTS 

Figure 3-4. Conceptual Representation of a Physiologically
 

Based Pharmacokinetic (PBPK) Model for a 

Hypothetical Chemical Substance
 

Inhaled chemical Exhaled chemical 

Ingestion 

Skin 

Kidney 

Richly 

perfused 

tissues 

Slowly 

perfused 

tissues 

Fat 

Liver 

Lungs 

V 

E 

N 

O 

U 

S 

B 

L 

O 

O 

D 

GI 

Tract 

Vmax Km 

Urine 

Chemicals in air 

contacting skin 

Feces 

A
 

R
 

T
 

E
 

R
 

I
 

A
 

L
 

B 

L 

O 

O 

D 

METHYL PARATHION 79 

Source: adapted from Krishnan et al. 1994 

Note: This is a conceptual representation of a physiologically based pharmacokinetic (PBPK) model for a hypothetical 

chemical substance. The chemical substance is shown to be absorbed via the skin, by inhalation, or by ingestion, 

metabolized in the liver, and excreted in the urine or by exhalation. 
METHYL PARATHION 80 

3. HEALTH EFFECTS 

No PBPK models were identified for methyl parathion. 

3.5 MECHANISMS OF ACTION 

3.5.1 Pharmacokinetic Mechanisms 

Based on the rapid appearance of clinical signs and cholinesterase inhibition, methyl parathion appears to 

be readily absorbed by humans and animals following inhalation, oral, and dermal exposure. Following 

oral administration of methyl parathion to animals, the extent of absorption was at least 77–80% 

(Braeckman et al. 1983; Hollingworth et al. 1967). No studies were located regarding the extent of 

absorption following inhalation and dermal exposure, or the mechanism of absorption. 

Data from a single study in dogs suggest that hepatic first-pass metabolism may limit systemic 

availability of the parent compound following oral exposure (Braeckman et al. 1983). Placental transfer 

of methyl parathion was demonstrated in pregnant rats 1–3 days before parturition. Thirty minutes after 

administration, both methyl parathion and methyl paraoxon were found in fetal brain, liver, and muscle; 

methyl parathion, but not methyl paraoxon, was detected in placenta and maternal liver (Ackermann and 

Engst 1970). Methyl parathion binds reversibly to serum albumin, but is readily distributed to the tissues 

(Braeckman et al. 1980, 1983). 

Methyl parathion is activated by desulfuration to its toxic metabolite, methyl paraoxon, by microsomal 

oxidases (cytochrome P-450) (Benke and Murphy 1975; Benke et al. 1974; Hollingworth et al. 1973; 

Nakatsugawa et al. 1968). The specific isozyme(s) that catalyze this reaction for the phosphorothioate 

esters, such as parathion and methyl parathion, do not appear to have been identified. Detoxification can 

occur through a number of pathways, including oxidation and removal of the aryl group from the parent 

compound, also mediated by microsomal oxidases (P-450 isozyme not known) (Benke and Murphy 1975; 

Benke et al. 1974; Nakatsugawa et al. 1968). Additional detoxification pathways include glutathionemediated dearylation of the parent compound, and hydrolysis or glutathione-mediated dealkylation or 

dearylation of methyl paraoxon (Benke and Murphy 1975; Benke et al. 1974). The importance of the 

glutathione-mediated pathways in vivo, however, is unclear (Chambers et al. 1994; Huang and Sultatos 

1993; Zhang and Sultatos 1991). An additional inactivating mechanism may be binding to tissue and 

plasma constituents (Benke and Murphy 1975), including plasma cholinesterase (Parkinson 1996), 

making methyl parathion unavailable. 
METHYL PARATHION 81 

3. HEALTH EFFECTS 

3.5.2 Mechanisms of Toxicity 

Almost all systemic effects of methyl parathion are related to the action of this compound on the nervous 

system or are secondary to this primary action. It is therefore necessary to preface a description of the 

mechanisms of toxicity of methyl parathion with a brief discussion of the nervous system and neurohumoral transmitters (excerpted from Lefkowitz et al. 1996). 

Neurohumoral transmitters are chemicals that facilitate the transmission of nerve impulses across nerve 

synapses and neuroeffector junctions. Acetylcholine is a neurohumoral transmitter that is present in the 

peripheral autonomic nervous system, in the somatic motor nervous system, and in some portions of the 

central nervous system. 

The autonomic nervous system is also called the involuntary nervous system; nerve fibers innervate heart, 

blood vessels, glands, various visceral organs, and smooth muscles. The autonomic nervous system is 

further divided into the parasympathetic and sympathetic systems. Both systems are involved in 

regulating the internal environment of the body and act in a contrasting manner. In general, the parasympathetic system is responsible for the maintenance of normal visceral organ functions including 

digestion and voiding; the sympathetic system has connections to the adrenal medulla and is geared for 

the body's "fight or flight" mechanisms. In the autonomic system, acetylcholine is a neurohumoral 

transmitter for all of the first set of neurons in this system (preganglionic fibers), for all of the second set 

of parasympathetic fibers (postganglionic fibers), and for a few postganglionic sympathetic fibers. These 

are all termed cholinergic fibers. 

The somatic motor nervous system or voluntary nervous system consists of nerve fibers that innervate 

skeletal muscle motor end-plates. 

Following release of acetylcholine at a nerve synapse or at a neuromuscular junction, the transmitter is 

rapidly hydrolyzed (within less than a millisecond) by an enzyme called acetylcholinesterase. This 

enzyme is present in high concentrations in cholinergic neurons and is localized at skeletal muscle endplates. Acetylcholinesterase is a highly efficient enzyme capable of hydrolyzing 6x105

 acetylcholine 

molecules per molecule of enzyme per minute (Taylor 1996). 

Acetylcholinesterase contained in erythrocytes is identical to that found in the nervous system. Its 

function within erythrocytes may be to control permeability of the cell membrane, to an extent. 
METHYL PARATHION 82 

3. HEALTH EFFECTS 

Functional neurological changes due to acute organophosphate exposure generally correlate with 

acetylcholinesterase inhibition in erythrocytes (Wills 1972). 

There is a second type of cholinesterase called butyrylcholinesterase, pseudocholinesterase, or 

cholinesterase. This enzyme is present in some nonneural cells in the central and peripheral nervous 

systems as well as in plasma and serum, the liver, and other organs. Its physiologic function is not 

known, but is hypothesized to be the hydrolysis of esters ingested from plants (Lefkowitz et al. 1996). 

Plasma cholinesterases are also inhibited by organophosphate compounds through irreversible binding; 

this binding can act as a detoxification mechanism as it affords some protection to acetylcholinesterase in 

the nervous system (Parkinson 1996; Taylor 1996). 

Methyl parathion and other organophosphates and their active metabolites exert their profound toxic 

effect by inhibiting the activity of acetylcholinesterase in the nervous system and at the motor end-plate. 

The active metabolite of methyl parathion, methyl paraoxon, inactivates acetylcholinesterase by phosphorylating the active site of the enzyme. The initial binding is somewhat reversible over a period of 

several hours, but over the following 24–48 hours, a process called “aging” occurs, resulting in the 

formation of a more stable covalent bond. Aging results from the removal of one of the alkyl side-chains 

of the phosphate group, leaving a hydroxyl group. This change prevents regeneration of the active 

enzyme, possibly by causing a conformational change that prevents the access of water for dephosphorylation, and represents an irreversible inhibition of the enzyme. Activity is regained only through the 

synthesis of new enzyme. Hydrolysis of acetylcholine is inhibited and the neurotransmitter accumulates 

at its site of action, producing overstimulation of cholinergic end organs, as described below (Proctor et 

al. 1988; Sultatos 1994; Taylor 1996). 

Clinical signs and symptoms of toxicity are related to the overstimulation of muscarinic, nicotinic, and 

central nervous system receptors in the nervous system. Muscarinic receptors are those activated by the 

alkaloid drug muscarine. These receptors are under the control of the parasympathetic nervous system, 

and their hyperactivity results in respiratory and gastrointestinal dysfunction, incontinence, salivation, 

bradycardia, miosis, and sweating. Nicotinic receptors are those activated by nicotine. Hyperactivity of 

these receptors results in muscle fasciculations; even greater stimulation results in blockade and muscle 

paralysis (Lefkowitz et al. 1996; Tafuri and Roberts 1987). Hyperactivity of central nervous system 

receptors results in the frank neurological signs of confusion, ataxia, dizziness, incoordination, and 

slurred speech, which are manifestations of acute intoxication. Muscarine and nicotine are not 
METHYL PARATHION 83 

3. HEALTH EFFECTS 

physiological stimulants, but rather are exogenous drugs that have been used experimentally to 

differentiate between the two types of receptors in the cholinergic system. 

The phenomenon of tolerance is well recognized in humans and other animal species after repeated 

exposure by various routes to sublethal doses of organophosphates (Costa et al. 1982). Typical 

cholinergic signs will occur after the initial exposure to an organophosphate; signs then diminish or 

disappear with continued dosing at the same level. A hypothetical mechanism for tolerance is downregulation, or decrease in the number of active muscarinic cholinergic receptors. Tolerance appears to be 

an adaptive response to organophosphate exposure. 

The mechanisms for the observed decrease in susceptibility of rats to the lethality of methyl parathion 

with increasing age may be age-related changes in metabolism. The deactivating pathways appear to 

increase, relative to the activating pathway, with increasing age from 1 to 60 days of age, leading to the 

hypothesis that detoxification pathways may be more effective in adult rats than in younger ones (Benke 

and Murphy 1975). These conclusions are based on the correlations of in vitro metabolism data with 

LD50 values; additional detail is provided in Section 3.3.3. 

In addition to effects mediated through glucocorticoid secretion (stress-related), a hypothetical 

mechanism for direct immunotoxicity of organophosphates is the inhibition of esterases and stabilization 

of the lysosomal membrane of lymphocytes, thus blocking release of lymphokines (Sharma and Reddy 

1987). 

3.5.3 Animal-to-Human Extrapolations 

Rigorous within-study comparisons of the toxicokinetics and health effects of methyl parathion in humans 

and experimental animals are generally not available, but across-study comparisons suggest that the 

kinetics and effects tend to be similar across species, with the following exception. The chicken, a test 

animal in studies of delayed neurotoxicity, is considered to be a good indicator species for delayed 

neurotoxicity. Treatment of chickens with methyl parathion did not cause signs of delayed neurotoxicity 

(Gaines 1969). Studies in rats, however, have indicated that intermediate or intermediate-to-chronic 

exposure to methyl parathion may result in decrements in nerve conduction (Desi et al. 1998) and in distal 

axonopathy (Suba 1984). The potential for methyl parathion to cause delayed neurotoxicity, and the 

relevance to humans of the negative findings in chickens versus the positive findings in rats, is unclear. 

This effect has not been observed in humans exposed to methyl parathion. 
METHYL PARATHION 84 

3. HEALTH EFFECTS 

3.6 ENDOCRINE DISRUPTION 

Recently, attention has focused on the potential hazardous effects of certain chemicals on the endocrine 

system because of the ability of these chemicals to mimic or block endogenous hormones, or otherwise 

interfere with the normal function of the endocrine system. Chemicals with this type of activity are most 

commonly referred to as endocrine disruptors. Some scientists believe that chemicals with the ability to 

disrupt the endocrine system are a potential threat to the health of humans, aquatic animals, and wildlife. 

Others believe that endocrine disrupting chemicals do not pose a significant health risk, particularly in 

light of the fact that hormone mimics exist in the natural environment. Examples of natural hormone 

mimics are the isoflavinoid phytoestrogens (Adlercreutz 1995; Livingston 1978; Mayr et al. 1992). These 

compounds are derived from plants and are similar in structure and action as endogenous estrogen. While 

there is some controversy over the public health significance of endocrine disrupting chemicals, it is 

agreed that the potential exists for these compounds to affect the synthesis, secretion, transport, binding, 

action, or elimination of natural hormones in the body that are responsible for the maintenance of 

homeostasis, reproduction, development, and/or behavior (EPA 1997). As a result, endocrine disruptors 

may play a role in the disruption of sexual function, immune suppression, and neurobehavioral function. 

Endocrine disruption is also thought to be involved in the induction of breast, testicular, and prostate 

cancers, as well as endometriosis (Berger 1994; Giwercman et al. 1993; Hoel et al. 1992). 

For methyl parathion, most of the information on health effects in humans is derived from cases of acute 

exposure to relatively high concentrations of the pesticide. Such reports have not addressed the issue of 

the potential endocrine-disrupting capacity of methyl parathion in humans. An added complication in 

determining whether methyl parathion has endocrine-disrupting capabilities in humans is the fact that 

humans are seldom exposed to a single pesticide. 

Studies in experimental animals have evaluated a wide array of relevant end points and the results have 

been mixed. For example, methyl parathion was not toxic to male germ cells from mice administered the 

test material in the diet or drinking water at up to the maximum tolerated dose (not specified) (Degraeve 

et al. 1985; Waters et al. 1982), but a later study showed that doses between 9.4 and 75 mg methyl 

parathion/kg increased the percentages of abnormal sperm cells in a dose-related manner (Mathew et al. 

1992). Repeated exposure of pregnant rats to an oral methyl parathion dose of 1.5 mg/kg, a dose that 

caused frank neurotoxicity, resulted in increased fetal resorptions (Gupta et al. 1984, 1985). Similar 

exposure of pregnant rats to 1 mg/kg/day of methyl parathion resulted in alterations in some behavioral 

end points in their offspring, evaluated at 2–6 months old (Gupta et al. 1985), suggesting that exposure in 
METHYL PARATHION 85 

3. HEALTH EFFECTS 

utero may lead to persistent effects; however, whether this may have been caused by an endocrinedisrupting mechanism cannot be determined. Similar results had been reported earlier by Crowder et al. 

(1980) following gavage administration of 1 mg/kg/day to pregnant rats. 

Intraperitoneal administration of a dose of 60 mg methyl parathion/kg to pregnant mice resulted in 

increased incidence of cleft palate in the fetuses and fetal deaths (Tanimura et al. 1967). In a more recent 

study, gavage administration of 1.5 mg methyl parathion/kg/day to rats on days 6–15 of gestation resulted 

in increased resorptions, decreased fetal body weight, and hemorrhagic spots in the brain ventricles and 

skin of the upper body of some of the fetuses (Kumar and Devi 1996). This dose level, however, also 

caused maternal toxicity expressed as cholinergic signs and depressed body weight gain. 

Decreased ovarian weight gain and inhibition of compensatory ovarian hypertrophy was observed in 

hemi-ovariectomized rats injected intraperitoneally with methyl parathion for 15 days at 5 mg/kg/day, in 

comparison with hemi-ovariectomized controls (Asmathbanu and Kaliwal 1997; Dhondup and Kaliwal 

1997). A decrease in the number of healthy follicles, no change in the number of atretic follicles, increase 

in duration of diestrus, decrease in the number of estrous cycles, and decrease in uterine weight also 

occurred in the methyl parathion-treated rats. Body weight gain was not decreased by methyl parathion, 

indicating that the effects were not due to nutritional deficiency. The effects of methyl parathion were not 

fully consistent with those of chlorinated pesticides that have estrogenic activity because methyl parathion 

did not increase follicular atresia, estrus duration, or uterine weight. 

Collectively, the findings in experimental animals are insufficient to categorize methyl parathion as an 

endocrine-disrupting chemical. 

The potential endocrine-disrupting capacity of methyl parathion in wildlife has also been examined, and 

results of some recent studies are summarized below. 

Exposure of two species of freshwater fish to 0.106 ppb of a commercial formulation containing 50% 

methyl parathion increased serum levels of T3 and reduced T4 (Bhattacharya 1993). This effect was 

attributed to inhibition of acetylcholinesterase activity in the fish brain, but no direct evidence was 

presented. Similar treatment of freshwater perch for 35 days resulted in decreased release of progesterone 

from the ovaries (Bhattacharya and Mondal 1997). Also, treatment of freshwater perch for up to 90 days 

with methyl parathion induced a decrease in the gonadosomatic index (not defined) after day 15 of 
METHYL PARATHION 86 

3. HEALTH EFFECTS 

exposure and in profiles of 17β-estradiol in serum and ovary that differed considerably from those in 

control animals over the exposure period (Choudhury et al. 1993). 

Exposure of male and female Japanese quail to 3, 12, or 48 ppm methyl parathion in the diet for 6 weeks 

throughout the laying period resulted in reduced number of eggs laid and in increased percentage of 

cracked eggs at the highest exposure level (Solecki et al. 1996). The highest exposure level also resulted 

in decreased plasma cholinesterase, whereas brain cholinesterase was reduced at all exposure levels. 

Neither fertility nor hatchability were affected by treatment. Oral treatment of wild passerine birds 

(Lonchura malabarica) with up to 200 μg methyl parathion/kg resulted in a significant reduction in testes 

weight at $100 μg/kg after 10 days of treatment (Maitra and Sarkar 1996). However, a single dose of 

50 μg/kg induced a significant decrease in the number of tubules containing healthy germ cells; the 

frequency and severity of this effect was dose-related and related to exposure duration. The authors also 

reported that effect on tubular germ cells was negatively correlated with acetylcholinesterase activity in 

the testes and brain and suggested that cholinergic activity may play a role in the influence of methyl 

parathion on gametogenic activities in the testes. Alternatively, they noted that brain cholinergic activity 

may also play a role through regulation of gonadotrophic secretion. 

In addition to in vivo tests, in vitro assays have been developed to test for hormone-mimicking properties 

of chemicals. These tests include cell proliferation assays and gene expression assays in mammalian cells 

and yeast. Although easy to conduct, these assays can yield both false negatives and false positives; for 

this reason, it is preferable to perform both in vivo and in vitro assays before classifying a chemical as to 

its endocrine-disrupting capacity. Limited information exists in this regard for methyl parathion. Methyl 

parathion exhibited very weak estrogenic properties (>10,000 times less potent than 17β-estradiol) in a 

yeast system expressing rainbow trout estrogen receptor (Petit et al. 1997). However, methyl parathion 

had an estrogenic potency similar to 17β-estradiol in a test in trout hepatocyte aggregate cultures that 

express the estrogen receptor (Petit et al. 1997). The structurally-related organophosphate pesticide, 

parathion, did not show estrogenic properties in breast cancer estrogen-sensitive MCF-7 cells (Soto et al. 

1995). 

In summary, while there is information on effects of methyl parathion that could be considered as 

endocrine-mediated, the less than optimal quality of the many of the studies do not allow for firm 

conclusions. Further research is needed to clarify whether methyl parathion may act as an endocrine 

disruptor. 
METHYL PARATHION 87 

3. HEALTH EFFECTS 

3.7 CHILDREN’S SUSCEPTIBILITY 

This section discusses potential health effects from exposures during the period from conception to 

maturity at 18 years of age in humans, when all biological systems will have fully developed. Potential 

effects on offspring resulting from exposures of parental germ cells are considered, as well as any indirect 

effects on the fetus and neonate resulting from maternal exposure during gestation and lactation. 

Relevant animal and in vitro models are also discussed. 

Children are not small adults. They differ from adults in their exposures and may differ in their 

susceptibility to hazardous chemicals. Children’s unique physiology and behavior can influence the 

extent of their exposure. Exposures of children are discussed in Section 6.6 Exposures of Children. 

Children sometimes differ from adults in their susceptibility to hazardous chemicals, but whether there is 

a difference depends on the chemical (Guzelian et al. 1992; NRC 1993). Children may be more or less 

susceptible than adults to health effects, and the relationship may change with developmental age 

(Guzelian et al. 1992; NRC 1993). Vulnerability often depends on developmental stage. There are 

critical periods of structural and functional development during both prenatal and postnatal life and a 

particular structure or function will be most sensitive to disruption during its critical period(s). Damage 

may not be evident until a later stage of development. There are often differences in pharmacokinetics 

and metabolism between children and adults. For example, absorption may be different in neonates 

because of the immaturity of their gastrointestinal tract and their larger skin surface area in proportion to 

body weight (Morselli et al. 1980; NRC 1993); the gastrointestinal absorption of lead is greatest in infants 

and young children (Ziegler et al. 1978). Distribution of xenobiotics may be different; for example, 

infants have a larger proportion of their bodies as extracellular water and their brains and livers are 

proportionately larger (Altman and Dittmer 1974; Fomon 1966; Fomon et al. 1982; Owen and Brozek 

1966; Widdowson and Dickerson 1964). The infant also has an immature blood-brain barrier (Adinolfi 

1985; Johanson 1980) and probably an immature blood-testis barrier (Setchell and Waites 1975). Many 

xenobiotic metabolizing enzymes have distinctive developmental patterns. At various stages of growth 

and development, levels of particular enzymes may be higher or lower than those of adults, and 

sometimes unique enzymes may exist at particular developmental stages (Komori et al. 1990; Leeder and 

Kearns 1997; NRC 1993; Vieira et al. 1996). Whether differences in xenobiotic metabolism make the 

child more or less susceptible also depends on whether the relevant enzymes are involved in activation of 

the parent compound to its toxic form or in detoxification. There may also be differences in excretion, 

particularly in newborns who all have a low glomerular filtration rate and have not developed efficient 
METHYL PARATHION 88 

3. HEALTH EFFECTS 

tubular secretion and resorption capacities (Altman and Dittmer 1974; NRC 1993; West et al. 1948). 

Children and adults may differ in their capacity to repair damage from chemical insults. Children also 

have a longer remaining lifetime in which to express damage from chemicals; this potential is particularly 

relevant to cancer. 

Certain characteristics of the developing human may increase exposure or susceptibility while others may 

decrease susceptibility to the same chemical. For example, although infants breathe more air per 

kilogram of body weight than adults breathe, this difference might be somewhat counterbalanced by their 

alveoli being less developed, which results in a disproportionately smaller surface area for alveolar 

absorption (NRC 1993). 

Present information indicates a potential for age-related differences in susceptibility to methyl parathion. 

However, data are limited in both human and animal studies. 

Acute exposure (via inhalation, dermal, and/or oral exposure routes) to methyl parathion has resulted in 

typical symptoms of organophosphate poisoning including depressed plasma and erythrocyte 

cholinesterase levels, altered function of nervous, cardiac, pulmonary, and gastrointestinal systems, and 

death in adults (Fazekas 1971; Fazekas and Rengei 1964) and children (Dean et al. 1984), indicating 

similarity in targets of toxicity from exposure to methyl parathion (see Section 3.5 for a more complete 

description of organophosphate poisoning). Toxicity in the nervous system is elicited by inhibition of the 

enzyme, acetylcholinesterase, which helps to control the level of the neurotransmitter acetylcholine. 

Lower levels of acetylcholinesterase result in effectively higher concentrations of acetylcholine and 

hyperactivity within the nervous system. 

Acetylcholine, acetylcholinesterase, and butyrylcholinesterase are involved in the development of the 

nervous system (Brimijoin and Koeninsberger 1999; Layer 1990; Layer and Willbold 1994); some of this 

development is not complete until adulthood. Therefore, toxic chemicals acting on these substances could 

cause deleterious developmental effects in addition to the typical physiological effects already discussed. 

Limited information regarding potential for age-related differences in susceptibility to methyl parathion in 

humans was reported by Dean et al. (1984). Seven children (ranging in age from 2 to 11 years) and 

three adults were exposed to unknown concentrations of methyl parathion sprayed illegally inside a house 

at a concentration of 4% (>3 times the recommended concentration for field applications). The children 
METHYL PARATHION 89 

3. HEALTH EFFECTS 

exhibited typical signs of organophosphate poisoning; two of them (4 and 11 years of age) died of 

respiratory arrest. Although the adults did not exhibit typical overt signs of methyl parathion poisoning, 

urinary levels of a methyl parathion metabolite (4-nitrophenol) were as high in the adults as in some of 

the children exhibiting toxic effects. The potential for age-related susceptibility could not be clearly 

assessed since critical information on individual exposure levels and routes was lacking. 

The only other information regarding the potential for age-related differences in susceptibility to methyl 

parathion came from a study by Garcia-Lopez and Monteoliva (1988). The investigators showed 

increasing mean erythrocyte acetylcholinesterase activity levels with increasing age range, starting at 

birth (in 10-year increments and >60 years of age) in both males and females. However, it is not known 

whether increased erythrocyte acetylcholinesterase activity indicates a decreased susceptibility to methyl 

parathion toxicity. 

Age-related differences in LD50 values for methyl parathion administered intraperitoneally have been 

shown in rats, with perinates being most susceptible and LD50 values increasing with age through adults 

(Benke and Murphy 1975; Kimmerle and Lorke 1968). The greatest change in LD50 values occurred in 

pups between 1 and 12–13 days old (Benke and Murphy 1975). While no significant age-related 

differences were noted in the in vitro inhibition of cholinesterase in brain homogenates treated with 

methyl paraoxon, in vitro metabolic studies of methyl parathion provide some evidence that age-related 

variation in a number of metabolic reactions might account, in part, for observed age-related changes in 

lethality. This age-related evidence includes positive correlations between changes in LD50 values for 

methyl parathion and ratios of oxidative deactivation (reaction 2 in Figure 3-3) to oxidative activation 

(reaction 1) of methyl parathion, as well as increases in hydrolysis (reaction 3), glutathion-dependent 

dealkylation and dearylation (reactions 5 and 7), and tissue binding of methyl paraoxon (Benke and 

Murphy 1975). The decreased susceptibility to methyl parathion toxicity (i.e., increased LD50 values) 

with increasing age was attributed to more effective detoxification in older rats relative to younger ones 

(Benke and Murphy 1975). However, in vivo studies have yet to confirm this hypothesis, and it is not 

known whether age-related differences in detoxification rates would play a role in low-level acute or 

chronic exposure scenarios. 

Pope et al. (1991) found that 7-day-old Sprague-Dawley rat pups were approximately twice as sensitive 

as 80–100-day-old adults to single subcutaneous doses of methyl parathion; the highest nonlethal dose 

7.8 mg/kg for the neonates and 18.0 mg/kg for adults. Initially, both neonates and adults exhibited 

similarly reduced brain acetylcholinesterase activity levels (approximately 10% that of controls); 
METHYL PARATHION 90 

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however, recovery of cholinesterase activity was more rapid in neonates (approximately 75% at 4 days 

posttreatment compared to only 30% in adults). In a subsequent study, Pope and Chakraborti (1992) 

showed that these age-related effects also occurred in a dose-related manner. Using daily subcutaneous 

dosing for 14 days, Liu et al. (1999) found that brain acetylcholinesterase activity was inhibited to a 

significantly greater extent in neonatal than in adult rats during dosing with 1.5 mg/kg/day, but that 

8 days after termination of exposure, there was little or no difference. The difference was diminished at a 

higher dose of 3 mg/kg/day, and recovery of activity was higher in the neonates after 8 days postexposure. Two other animal studies reported age-related responses to methyl parathion exposure by the 

oral route. Kumar and Desiraju (1992) found no statistically significant difference in the magnitude of 

brain acetylcholinesterase inhibition in 15-day-old Wistar rat pups and 90-day-old adults (approximately 

47 and 60%, respectively) following single oral (gavage) doses of 1 mg/kg. 

Placental transfer of methyl parathion was demonstrated in pregnant rats after oral administration of 

11.1 mg methyl parathion/kg body weight (Ackermann and Engst 1970). Following sacrifice 30 minutes 

posttreatment, maternal liver and placenta were found to contain measurable amounts of methyl 

parathion, but not methyl paraoxon. Fetal brain, liver, and muscle tissues contained methyl parathion 

concentrations up to approximately 2.5 times that of the maternal liver. Similarly, placental transfer was 

demonstrated in pregnant rats following dermal application of 10 mg methyl parathion/kg (Abu-Qare et 

al. 2000). By 4 hours postadministration, the highest concentration of methyl parathion was found in 

fetal tissue; the concentration in placental tissue was about as high as that of the maternal liver. Fish 

(1966) gave supporting evidence for placental transfer of methyl parathion and/or its toxic metabolites by 

demonstrating that brain cholinesterase activity was reduced in fetal rats following intraperitoneal 

injections of the pregnant dams with maternally-toxic doses of methyl parathion. Methyl parathion was 

found in breast milk in a limited number of samples from women of central Asia, for which exposure data 

were not available (Lederman 1996) (see also Section 3.4.2.2). This indicates that methyl parathion 

might be transferred from contaminated mother to nursing infant. No information was locating regarding 

the presence of methyl parathion metabolites in breast milk. A study of a mixture of pesticides (methyl 

parathion, lindane, and permethrin) in rats reported that following oral exposure of the dams on lactation 

days 1–14, methyl parathion was present in higher concentrations in their milk and in the pups’ blood 

than in the dams’ blood (Golubchikov 1991; Goncharuk et al. 1990). Confidence in this study is low 

because descriptions of the methods and results were cursory. 
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It is not presently known what phase I enzymes metabolize methyl parathion, and consequently, whether 

metabolism differs between children and human adults. There is some suggestive evidence for agerelated differences in metabolism of methyl parathion in rats (Benke and Murphy 1975). 

Tanimura et al. (1967) reported increased incidences of cleft palate and mortality in fetuses of pregnant 

mice injected intraperitoneally with 60 mg methyl parathion/kg. Significantly reduced maternal and fetal 

brain acetylcholinesterase activity, increased resorptions (Gupta et al. 1985), and dose-related reductions 

in net maternal and fetal protein synthesis (Gupta et al. 1984) were noted following oral exposure of 

pregnant rats to methyl parathion during gestation. Crowder et al. (1980) reported increased mortality in 

rat pups (relative to controls) following oral administration of methyl parathion to pregnant dams during 

gestation and a significant difference in maze transfer tests between treatment and control groups. Kumar 

and Devi (1996) also reported treatment-related maternal and fetal effects in rats following oral 

administration of methyl parathion to dams during gestation. However, there were no reports of agerelated differences in susceptibility to methyl parathion in any of these studies. 

Dose-related changes on electrocorticograms and on nerve conduction velocity and refractory period were 

reported in rats that were exposed to methyl parathion via treatment of the dams during gestation and 

lactation, and then orally at dose levels of 0.22, 0.44, or 0.88 mg/kg/day for 8 more weeks of postnatal 

development to the age of 12 weeks (Desi et al. 1998). These effects were not seen in 12-week-old rats 

following exposure only during gestation and lactation or gestation alone. No overt toxic signs were seen 

in dams or offspring. 

3.8 BIOMARKERS OF EXPOSURE AND EFFECT 

Biomarkers are broadly defined as indicators signaling events in biologic systems or samples. They have 

been classified as markers of exposure, markers of effect, and markers of susceptibility (NAS/NRC 1989). 

Due to a nascent understanding of the use and interpretation of biomarkers, implementation of biomarkers 

as tools of exposure in the general population is very limited. A biomarker of exposure is a xenobiotic 

substance or its metabolite(s), or the product of an interaction between a xenobiotic agent and some target 

molecule(s) or cell(s) that is measured within a compartment of an organism (NAS/NRC 1989). The 

preferred biomarkers of exposure are generally the substance itself or substance-specific metabolites in 

readily obtainable body fluid(s) or excreta. However, several factors can confound the use and 
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interpretation of biomarkers of exposure. The body burden of a substance may be the result of exposures 

from more than one source. The substance being measured may be a metabolite of another xenobiotic 

substance (e.g., high urinary levels of phenol can result from exposure to several different aromatic 

compounds). Depending on the properties of the substance (e.g., biologic half-life) and environmental 

conditions (e.g., duration and route of exposure), the substance and all of its metabolites may have left the 

body by the time samples can be taken. It may be difficult to identify individuals exposed to hazardous 

substances that are commonly found in body tissues and fluids (e.g., essential mineral nutrients such as 

copper, zinc, and selenium). Biomarkers of exposure to methyl parathion are discussed in Section 3.8.1. 

Biomarkers of effect are defined as any measurable biochemical, physiologic, or other alteration within an 

organism that, depending on magnitude, can be recognized as an established or potential health 

impairment or disease (NAS/NRC 1989). This definition encompasses biochemical or cellular signals of 

tissue dysfunction (e.g., increased liver enzyme activity or pathologic changes in female genital epithelial 

cells), as well as physiologic signs of dysfunction such as increased blood pressure or decreased lung 

capacity. Note that these markers are not often substance specific. They also may not be directly 

adverse, but can indicate potential health impairment (e.g., DNA adducts). Biomarkers of effects caused 

by methyl parathion are discussed in Section 3.8.2. 

A biomarker of susceptibility is an indicator of an inherent or acquired limitation of an organism's ability 

to respond to the challenge of exposure to a specific xenobiotic substance. It can be an intrinsic genetic 

or other characteristic or a preexisting disease that results in an increase in absorbed dose, a decrease in 

the biologically effective dose, or a target tissue response. If biomarkers of susceptibility exist, they are 

discussed in Section 3.10 Populations That Are Unusually Susceptible. 

3.8.1 Biomarkers Used to Identify or Quantify Exposure to Methyl Parathion 

The most specific biomarker of exposure to methyl parathion is the presence of the compound in serum or 

tissue. This is an especially good biomarker for detection shortly after acute exposure. For example, 

methyl parathion levels were detected in the sera of five men who were exposed for 5 hours in a cotton 

field 12 hours after it was sprayed with methyl parathion. The route of exposure was dermal, through 

unprotected hands. Serum levels averaged 156 ppb after 3 hours of the 5-hour exposure, and averaged 

101.4 and 2.4 ppb at 7 and 24 hours postexposure, respectively (Ware et al. 1975). 
METHYL PARATHION 93 

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These results are supported by studies in animals in which methyl parathion was detected 30–155 minutes 

after exposure (oral, dermal, inhalation, or intravenous routes) in plasma and liver (Abu-Qare et al. 2000; 

EPA 1978e). Due to extensive and rapid metabolism of methyl parathion (see Section 3.3), measurable 

levels are not expected to persist in tissue or serum for prolonged periods after exposure. 

Urine of exposed humans can also be monitored for two metabolites of methyl parathion: 4-nitrophenol 

(measured after hydrolysis of the glucuronide, Section 3.3.4) and dimethyl phosphate. After ingestion of 

2 or 4 mg of methyl parathion, maximum urinary excretion occurred as follows: 4-nitrophenol within 

4 hours, and dimethyl phosphate between 4 and 8 hours. Metabolites were not detected in urine on the 

second day after exposure (Morgan et al. 1977). Metabolites, such as 4-nitrophenol, have also been 

detected in stomach contents, urine, and tissues of humans committing suicide by ingestion of methyl 

parathion (Fazekas 1971). These metabolites are not, however, specific for methyl parathion. The 

metabolite 4-nitrophenol can also occur as a breakdown product of other organophosphate insecticides 

such as parathion as well as some nonorganophosphate compounds, while alkylphosphates are metabolic 

end-products of most organophosphates (Davies and Peterson 1997; Morgan et al. 1977). 

Urinary 4-nitrophenol was detected in intoxicated children and clinically normal adults in a household 

where there had been exposure to methyl parathion (Dean et al. 1984). 

Associations between urinary 4-nitrophenol and indoor residential air and surface-wipe concentrations of 

methyl parathion have been studied in 142 residents of 64 contaminated homes in Lorain, Ohio (Esteban 

et al. 1996). The homes were contaminated through illegal spraying. A mathematic model was 

developed to evaluate the association between residential contamination and urinary 4-nitrophenol. There 

were significant positive correlations between air concentration and urinary 4-nitrophenol, and between 

maximum surface-wipe concentrations and urinary 4-nitrophenol. The final model includes the following 

variables: number of days between spraying and sample collection, air and maximum surface wipe 

concentration, and age, and could be used to predict urinary 4-nitrophenol. 

3.8.2 Biomarkers Used to Characterize Effects Caused by Methyl Parathion 

Diagnosis of organophosphate poisoning (including methyl parathion) can be confirmed by evaluation of 

serum (plasma) cholinesterase and erythrocyte cholinesterase. However, cholinesterase inhibition is not 

specific for organophosphates. For example, carbamate insecticides also result in cholinesterase 

inhibition, which is usually transitory. Erythrocyte cholinesterase measurement is a specific test for 
METHYL PARATHION 94 

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acetylcholinesterase inhibition since it is found in both the peripheral and central nervous systems. 

However, measurement is complicated by the fact that normal erythrocyte cholinesterase values 

encompass a broad range in the human population (Midtling et al. 1985; Tafuri and Roberts 1987). 

Serum cholinesterase (pseudocholinesterase) is a more sensitive but less specific indicator of organophosphate toxicity since the levels may also be suppressed due to genetic factors and to a variety of 

conditions and diseases (Henry 1984; Tafuri and Roberts 1987). Acetylcholinesterase activity recovers as 

a result of the synthesis of new enzyme and recovery generally occurs at a rate of approximately 1% per 

day. However, the symptoms of methyl parathion poisoning usually resolve more rapidly. Therefore, 

even if they are symptom-free, persons poisoned by methyl parathion may have lowered cholinesterase 

levels for a month after exposure and should avoid re-exposure for several weeks (Proctor et al. 1988). 

Also, normal values may have interlaboratory variation (NIOSH 1976). Several field tests for measuring 

erythrocyte acetylcholinesterase and plasma cholinesterase are available (Wills 1972). Baseline data are 

often collected for workers, but these data would not be available for environmentally exposed people. 

Sequential determinations of cholinesterase levels from individuals probably exposed to methyl parathion 

could be an alternative method of determining cholinesterase inhibition (Midtling et al. 1985). In 

interpreting results, it should be noted that there are both age- and gender-related differences in normal 

erythrocyte and plasma cholinesterase levels in humans (Garcia-Lopez and Monteoliva 1988; Wills 

1972). See Sections 3.7 and 3.10 for additional information on these age- and gender-related differences. 

A classification of organophosphate poisoning has been proposed by Tafuri and Roberts (1987) modified 

from Namba et al. (1971). Clinical signs and symptoms of intoxication may occur when serum 

cholinesterase levels drop to below 50% of the normal value. Mild poisoning, with the patient still 

ambulatory, may occur when serum cholinesterase levels are 20–50% of normal; moderate poisoning with 

inability to walk with levels 10–20% of normal; and severe poisoning with respiratory distress and 

unconsciousness with serum cholinesterase levels <10% of normal. 

Following exposure of humans to organophosphates, but not specifically methyl parathion, restoration of 

plasma cholinesterase occurs more rapidly than does restoration of erythrocyte cholinesterase (Grob et 

al. 1950; Midtling et al. 1985). These findings are supported by studies of methyl parathion in animals. 

Erythrocyte cholinesterase levels are representative of acetylcholinesterase levels in the nervous system, 

and, therefore, may be a more accurate biomarker of the neurological effects of chronic low level 

exposure of humans to methyl parathion (Midtling et al. 1985; NIOSH 1976). 
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3.9 INTERACTIONS WITH OTHER CHEMICALS 

Emergency therapy of acute organophosphate (including methyl parathion) intoxication in humans and 

other mammals relies on the antagonistic interactions of several drugs. Atropine serves as a potent 

antidote by blocking the action of acetylcholine at muscarinic nerve receptors and, therefore, lessens 

clinical signs related to parasympathetic stimulation caused by the inactivation of acetylcholinesterase by 

methyl parathion. 2-Pyridine aldoxime methiodide (2-PAM) reverses the effect of cholinergic nicotinic 

stimulation such as at the motor nerve junctions with the end-plates of skeletal muscle fibers. This 

treatment ameliorates signs and symptoms of skeletal muscle fasciculation, muscle weakness, and lifethreatening paralysis of respiratory muscles. 2-PAM is able to reactivate phosphorylated cholinesterase if 

the drug is administered within 24–36 hours of acute methyl parathion intoxication. After that time, 

irreversible changes in the phosphorylated enzyme occur, and 2-PAM is ineffective as an antidote (Tafuri 

and Roberts 1987). 

Compounds that affect activities of hepatic microsomal enzymes can antagonize the effects of methyl 

parathion, presumably by decreasing metabolism of methyl parathion to methyl paraoxon or enhancing 

degradation to relatively nontoxic metabolites. For example, pretreatment with phenobarbital protected 

rats from methyl parathion's cholinergic effects (Murphy 1980) and reduced inhibition of acetylcholinesterase activity in the rat brain (Tvede et al. 1989). Phenobarbital pretreatment prevented lethality 

from methyl parathion in mice compared to saline-pretreated controls (Sultatos 1987). Pretreatment of 

rats with two other pesticides, chlordecone or mirex, also reduced inhibition of brain acetylcholinesterase 

activity in rats dosed with methyl parathion (2.5 mg/kg intraperitoneally), while pretreatment with the 

herbicide linuron decreased acetylcholine brain levels below those found with methyl parathion treatment 

alone (Tvede et al. 1989). 

Cimetidine, an H2 antagonist used therapeutically in patients with ulcers, inhibits activity of hepatic 

microsomal enzymes. When rats or mice were pretreated with cimetidine, dose-related lethality of methyl 

parathion was reduced, and cholinergic signs of toxicity were delayed. Simultaneous administration with 

methyl parathion did not reduce toxicity (Joshi and Thornburg 1986). 

Piperonyl butoxide, a common potentiator of insecticide effects that inhibits microsomal enzymes, 

antagonized the toxic effects of methyl parathion in mice (Mirer et al. 1977). 
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Gentamicin is a broad spectrum aminoglycoside antibiotic, and rifamycin is an antituberculosis drug. 

Pretreatment of rats with these agents protected them against toxic effects of a single oral dose of methyl 

parathion. Plasma cholinesterase and liver carboxylesterase levels were higher in pretreated than 

untreated rats challenged with methyl parathion. Pretreated rats had significantly decreased methyl 

paraoxon levels in liver and skeletal muscles while 4-nitrophenol levels were increased in the urine, 

indicative of enhanced detoxification (Youssef et al. 1987). 

Acetaminophen, which depletes hepatic glutathione, does not potentiate the toxicity of methyl parathion 

in mice. A possible mechanism of action may be competition between acetaminophen and methyl 

parathion for mixed function oxidases and subsequent prevention of activation of methyl parathion to 

methyl paraoxon (Costa and Murphy 1984). Diethyl maleate, an agent that depletes cytosolic glutathione 

and is not an enzyme inducer, potentiates toxicity of methyl parathion in mice (Mirer et al. 1977). 

Permethrin, a pyrethrin pesticide, decreased the inhibition of brain cholinesterase activity by methyl 

parathion, but methyl parathion decreased the LD50 of permethrin when the two pesticides were 

simultaneously administered to rats (Ortiz et al. 1995). The potentiation of permethrin lethality may be 

due to the inhibition by methyl parathion of carboxylesterase, which metabolizes permethrin. 

3.10 POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE 

A susceptible population will exhibit a different or enhanced response to methyl parathion than will most 

persons exposed to the same level of methyl parathion in the environment. Reasons may include genetic 

makeup, age, health and nutritional status, and exposure to other toxic substances (e.g., cigarette smoke). 

These parameters result in reduced detoxification or excretion of methyl parathion, or compromised 

function of organs affected by methyl parathion. Populations who are at greater risk due to their 

unusually high exposure to methyl parathion are discussed in Section 6.7 Populations With Potentially 

High Exposures. 

Unusually susceptible populations are those groups of individuals who respond more quickly or at lower 

exposure levels than the general population to the toxic effects of methyl parathion. These responses may 

be genetic in origin or may be due to differences in development or life style factors such as nutrition or 

behavior, or due to preexisting disease states. 
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People who should not work with organophosphate insecticides are those with organic central nervous 

system disease, mental disorders, epilepsy, pronounced endocrine disorders, respiratory conditions, 

cardiovascular diseases, circulatory disorders, gastroenteric diseases, liver or kidney disease, and chronic 

conjunctivitis and keratitis (Medved and Kagan 1983). 

Individuals with hereditary low plasma cholinesterase levels (Kalow 1956; Lehman and Ryan 1956) and 

those with paroxysmal nocturnal hemoglobinuria, which is related to abnormally low levels of 

erythrocyte acetylcholinesterase (Auditore and Hartmann 1959), would have increased susceptibility to 

the effects of anticholinesterase agents such as methyl parathion. Repeated measurements of plasma 

cholinesterase activity (in the absence of organophosphate exposure) can be used to identify individuals 

with genetically determined low plasma cholinesterase. 

Women have exhibited significantly decreased plasma cholinesterase levels (De Peyster et al. 1994; 

Evans and Wroe 1980; Evans et al. 1988; Howard et al. 1978; Sanz et al. 1991; Venkataraman et al. 1990) 

and significantly increased erythrocyte acetylcholinesterase levels (De Peyster et al. 1994; Sanz et al. 

1991; Venkataraman et al. 1990) during pregnancy. It is not known whether these differences might 

make pregnant women more susceptible to methyl parathion toxicity. 

Several studies in animals suggest that age may affect susceptibility to methyl parathion toxicity, and that 

children may be more susceptible than adults, but the data are limited. (See Section 3.7 for more 

information on Children’s susceptibility.) A study in humans showed that mean erythrocyte acetylcholinesterase activity levels increase with increasing age from birth through old age in both sexes 

(Garcia-Lopez ad Monteoliva 1988), but it is not known whether increased erythrocyte acetylcholinesterase activity indicates decreased susceptibility to methyl parathion. 

Male rodents have been shown to be more susceptible to acute toxic effects of methyl parathion than 

females (EPA 1978e; Murphy and Dubois 1958). 

3.11 METHODS FOR REDUCING TOXIC EFFECTS 

This section will describe clinical practice and research concerning methods for reducing toxic effects of 

exposure to methyl parathion. However, because some of the treatments discussed may be experimental 

and unproven, this section should not be used as a guide for treatment of exposures to methyl parathion. 

When specific exposures have occurred, poison control centers and medical toxicologists should be 
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consulted for medical advice. The following texts provide specific information about treatment following 

exposures to methyl parathion: 

Aaron CK, Howland, MA. 1998. Insecticides: Organophosphates and carbamates. In: Goldfrank LR, 

Flomenbaum NE, Lewin NA, et al., eds. Goldfrank's toxicologic emergencies. Stamford, CT: Appleton 

& Lange, 1429–1449. 

Bronstein AC, Currance PL, eds. 1988. Emergency care for hazardous materials exposure. St. Louis, 

MO: CV Mosby Company, 66, 199–200. 

Ellenhorn MJ. 1997. Pesticides: Insecticides. In: Ellenhorn’s medical toxicology: Diagnosis and 

treatment of human poisoning. Baltimore, MD: Williams & Wilkins, 1614–1631. 

EPA. 1989b. Recognition and management of pesticide poisonings. 4th ed. Washington, DC: U.S. 

Environmental Protection Agency. Health Effects Division. Office of Pesticide Programs. EPA 

540/9-88-001. 

3.11.1 Reducing Peak Absorption Following Exposure 

Procedures that have been used to reduce absorption of methyl parathion include the following. In 

inhalation and dermal exposures, the exposed person is first removed from the source of exposure. 

Dermal absorption is then reduced by washing the skin and hair with mild soap or detergent and copious 

amounts of water. If immediately available, a mild hypochlorite (bleach) solution can be used on the skin 

(not in the eyes); the chlorine radical deactivates organophosphate agents. Care is taken to avoid abrading 

the skin as methyl parathion may be more rapidly absorbed through cuts, cracks, or abrasions in the skin 

(Aaron and Howland 1998). Ocular absorption is limited by irrigating the eyes with copious amounts of 

normal saline or lactated Ringer’s solution, or, if these solutions are not available, water (Aaron and 

Howland 1998; Stutz and Janusz 1988). After acute oral exposures to high doses, absorption from the 

gastrointestinal tract is limited by gastric lavage followed by administration of activated charcoal to 

absorb residual methyl parathion present in the gut. Emesis with ipecac has been discouraged because 

coma or seizures may develop rapidly in acute high-dose situations (Aaron and Howland 1998). In lowdose situations, where swallowing is not impaired and a good gag reflex and no drooling exist, absorption 

of methyl parathion from the gastrointestinal tract may be limited by drinking water to dilute the contents 

of the gastrointestinal tract (Bronstein and Currance 1988), but this procedure will expose a larger area of 

absorptive surface to the toxicant. 
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3.11.2 Reducing Body Burden 

No information was located regarding methods for reducing body burden of methyl parathion. 

3.11.3 Interfering with the Mechanism of Action for Toxic Effects 

Methyl parathion produces its toxic effects by inhibiting acetylcholinesterase. This results in excess 

acetylcholine at the synapses and neuroeffector junctions. Treatment of methyl parathion poisoning is 

directed toward reducing the effects of the excess acetylcholine and reactivating acetylcholinesterase. 

Atropine may be given to block muscarinic cholinergic receptors and limit the action of acetylcholine at 

this class of receptors. In cases of moderately severe poisoning, a state of atropinization (tachycardia, 

flushing, dry mouth, dilated pupils) is maintained for extended periods (Aaron and Howland 1998; 

Ellenhorn 1997; Proctor et al. 1988). Pralidoxime (2-PAM) acts to reactivate acetylcholinesterase and is 

given in conjunction with atropine therapy. It is most effective if administered shortly after exposure to 

methyl parathion because the inhibited acetylcholinesterase molecule becomes resistant to reactivation 

(aging) within several hours (24–36 hours). Therapy with 2-PAM is continued for at least 18 hours 

(Aaron and Howland 1998; Ellenhorn 1997; EPA 1989b). However, prophylactic administration of 

atropine and/or 2-PAM prior to organophosphate exposure is not recommended (EPA 1989b). The 

intermediate syndrome, which has been reported for some organophosphate pesticides, including a 

mixture of parathion and methyl parathion, may cause respiratory insufficiency or arrest 1–4 days after 

resolution of the acute cholinergic crisis. Therefore, patients exposed to organophosphates associated 

with this syndrome are observed for a more prolonged period of time, and may be continued on 2-PAM 

therapy after resolution of the cholinergic crisis (Aaron and Howland 1998). 

Following inhibition by methyl parathion, acetylcholinesterase activity recovers as a result of the 

synthesis of new enzyme, generally at a rate of approximately 1% per day. However, the symptoms of 

methyl parathion poisoning usually resolve much more rapidly. Therefore, even though they are 

symptom-free, persons poisoned by methyl parathion may be hypersusceptible to its effects and should 

avoid reexposure for several weeks (Aaron and Howland 1998; Proctor et al. 1988). 
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3.12 ADEQUACY OF THE DATABASE 

Section 104(i)(5) of CERCLA, as amended, directs the Administrator of ATSDR (in consultation with the 

Administrator of EPA and agencies and programs of the Public Health Service) to assess whether 

adequate information on the health effects of methyl parathion is available. Where adequate information 

is not available, ATSDR, in conjunction with the National Toxicology Program (NTP), is required to 

assure the initiation of a program of research designed to determine the health effects (and techniques for 

developing methods to determine such health effects) of methyl parathion. 

The following categories of possible data needs have been identified by a joint team of scientists from 

ATSDR, NTP, and EPA. They are defined as substance-specific informational needs that if met would 

reduce the uncertainties of human health assessment. This definition should not be interpreted to mean 

that all data needs discussed in this section must be filled. In the future, the identified data needs will be 

evaluated and prioritized, and a substance-specific research agenda will be proposed. 

3.12.1 Existing Information on Health Effects of Methyl Parathion 

The existing data on health effects of inhalation, oral, and dermal exposure of humans and animals to 

methyl parathion are summarized in Figure 3-5. The purpose of this figure is to illustrate the existing 

information concerning the health effects of methyl parathion. Each dot in the figure indicates that one or 

more studies provide information associated with that particular effect. The dot does not necessarily 

imply anything about the quality of the study or studies, nor should missing information in this figure be 

interpreted as a “data need”. A data need, as defined in ATSDR’s Decision Guide for Identifying 

Substance-Specific Data Needs Related to Toxicological Profiles (ATSDR 1989), is substance-specific 

information necessary to conduct comprehensive public health assessments. Generally, ATSDR defines a 

data gap more broadly as any substance-specific information missing from the scientific literature. 

Figure 3-5 graphically depicts the information that currently exists on the health effects of methyl 

parathion in humans and animals by various routes of exposure. The available literature reviewed 

concerning the health effects of methyl parathion in humans described case reports of longer-term studies 

of pesticide workers and case reports of accidental or intentional ingestion of methyl parathion. The 

occupational exposure is believed to be via the dermal and inhalation routes. The information on human 

exposure is limited in that the possibility of concurrent exposure to other pesticides or other toxic 

substances cannot be quantified. 
METHYL PARATHION 101 

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Figure 3-5. Existing Information on Health Effects of Methyl Parathion 
 

METHYL PARATHION 102 

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The database for the health effects of methyl parathion after ingestion in experimental animals is 

substantial. However, as can be seen in Figure 3-5, only limited information is available on the effects of 

inhalation and dermal exposure to methyl parathion in animals. Furthermore, the health effects such as 

death and neurotoxicity resulting from acute exposure in animals are more fully studied than systemic and 

immunotoxic effects associated with acute exposure. 

3.12.2 Identification of Data Needs 

Acute-Duration Exposure. Information is available regarding acute-duration exposure in humans 

and animals following exposure by all three routes. However, the studies in humans via the inhalation 

and dermal routes involved combined exposure by both routes (Dean et al. 1984; Fazekas 1971). Acute 

ingestion of high doses and combined exposure to methyl parathion via inhalation and dermal routes 

result primarily in neurological and systemic effects in humans (Dean et al. 1984; Fazekas 1971; Fazekas 

and Rengei 1964). However, exposure levels in these studies were not quantified. An experimental study 

in humans at very low oral doses resulted in no neurological effects, but involved only two subjects, and 

no concurrent controls (Rodnitzky et al. 1978). The target of toxicity in humans and animals following 

acute, high-level exposure by any route is the nervous system (Dean et al. 1984; EPA 1978e; Miyamoto 

et al. 1963b; Yamamoto et al. 1982; Youssef et al. 1987). The observed effects on the liver (Fazekas 

1971; Fazekas and Rengei 1964; Sonnenschein et al. 1989a, 1989b) and respiratory (EPA 1978e; Fazekas 

1971) systems may be primary or secondary effects of methyl parathion toxicity following acute oral 

exposure in experimental animals. The observed effects have also been seen in humans from oral 

exposure and from combined exposure by the inhalation and dermal routes (Fazekas 1971; Fazekas and 

Rengei 1964). For the oral route, the highest NOAEL below a LOAEL was 0.88 mg/kg/day for 

developmental effects in rats (Desi et al. 1998), and this dose level was too close to a serious LOAEL of 

1 mg/kg/day for neurodevelopmental effects in rats (Crowder et al. 1980) to be used for MRL derivation. 

Additional acute oral studies that could provide dose-response information at low exposure levels are 

needed. Only qualitative human data (exposure level and duration not quantified) and animal LC50 data 

are available for the inhalation route of exposure (Dean et al. 1984; Fazekas 1971; Kimmerle and Lorke 

1968). No dose-response data are available. Data on neurological effects in humans or animals are not 

sufficient to derive an acute inhalation MRL (Dean et al. 1984; EPA 1978e). Therefore additional 

inhalation studies are needed. The available toxicokinetic data are not adequate to predict the behavior of 

methyl parathion across the routes of exposure. The limited toxicity information available indicates that 

similar effects are observed (i.e., death, neurotoxicity) in both animals (EPA 1978e; Miyamoto et al. 

1963b; Nemec et al. 1968; Yamamoto et al. 1982; Youssef et al. 1987) and humans (Dean et al. 1984; 
 

METHYL PARATHION 103 

3. HEALTH EFFECTS 

Fazekas 1971) exposed by various routes. Because of a lack of toxicokinetic data, it cannot be assumed 

that the end points of methyl parathion toxicity would be quantitatively similar across all routes of 

exposure. The acute effects of dermal exposures to methyl parathion are not well characterized in humans 

or animals. Therefore, additional dermal studies are needed. 

Intermediate-Duration. No information is available on the toxicity of methyl parathion to humans 

following intermediate-duration exposure by any route. In an oral study in humans, 30 mg of methyl 

parathion administered to adult males daily for 30 days depressed erythrocyte cholinesterase levels to 

37% of preexposure values; this abstract did not indicate whether toxicity was produced (Rider et 

al. 1971). Information is available regarding intermediate-duration exposure in animals following oral 

exposure; toxicity in animals is manifested by neurological (Daly 1989; Desi et al. 1998; Williams et al. 

1959), gastrointestinal (NCI 1979), developmental (Gupta et al. 1985), and immunological (Shtenberg 

and Dzhunusova 1968; Street and Sharma 1975) effects. An intermediate-duration gavage study of 

methyl parathion in rats identified hematological effects of anemia (decreased erythrocyte count and 

hematocrit) and slight leukocytosis with neutropenia and lymphocytosis (Galal et al. 1977). However, 

this study had severe limitations (i.e., a dosing design which did not allow establishing effect levels) that 

precluded its use. These limitations included increases in dose every 4 days, lack of controls, abnormal 

before-treatment values, irregularities in calculations, and disparities between the text and tables. A more 

reliable intermediate-duration gavage study in rats found no change in leukocyte counts or differential 

counts (Crittenden et al. 1998). Nevertheless, because erythrocyte cholinesterase has an action of 

controlling erythrocyte permeability (Wills 1972), experimental data on the hematological effects of 

intermediate-duration exposure to methyl parathion are needed. The oral exposure data in animals from 

the Desi et al. (1998) study are sufficient to derive an intermediate oral MRL based on adverse neurological effects. Additional studies examining the dose-response and critical periods for neurobehavioral 

developmental effects of intermediate-duration oral exposure to methyl parathion are needed. Since no 

data are available for the inhalation route of exposure, an intermediate inhalation MRL could not be 

derived. The available toxicity data are not adequate to predict the behavior of methyl parathion across 

routes of exposure. The limited toxicity information available indicates that similar effects are observed 

(i.e., neurotoxic) in animals following oral, inhalation, or dermal exposure. However, it cannot be 

assumed that the end points of methyl parathion toxicity are quantitatively similar across all routes of 

exposure, and, therefore, it may not be possible to predict the levels that cause these effects by all routes 

of exposure. The dermal and inhalation studies of intermediate duration are needed to identify more 

accurately the end points of toxicity and the levels at which these effects are observed. 
 

 

METHYL PARATHION 104 

3. HEALTH EFFECTS 

Chronic-Duration Exposure and Cancer. No information is available on the toxicity of methyl 

parathion in humans following chronic-duration exposure by any route. The oral exposure data in 

animals from the Suba (1984) study are sufficient to derive a chronic oral MRL based on adverse 

hematological effects (Suba 1984). No chronic-duration exposure data are available for the inhalation or 

dermal routes of exposure. Therefore, no MRL for a chronic exposure duration could be derived for the 

inhalation route. No data regarding potential hematological effects of inhalation or dermal exposure are 

available for any duration. Because other effects of methyl parathion, such as neurological effects, are 

seen for all three routes of exposure, hematological effects also may occur following inhalation or dermal 

exposure; additional testing is needed. The toxicity information available for acute-duration exposures 

indicate that similar effects are observed in the central nervous system from oral, inhalation, and dermal 

exposures. Neurological effects were observed in chronic oral exposure (Suba 1984). Additional data are 

needed to determine whether chronic inhalation exposures by the dermal and inhalation routes also affect 

the nervous system. Additional studies are needed to identify end points, in addition to the hematological 

and nervous systems, that are affected by chronic exposures via each of these routes, and the levels at 

which these effects would be observed. 

No reports of cancer in humans associated with exposure to methyl parathion by any route have been 

found. The carcinogenicity of methyl parathion has been studied in two chronic oral bioassays using rats 

(NCI 1979; Suba 1984) and mice (NCI 1979). The available data in experimental animals are negative. 

However, limitations associated with the study by NCI (i.e., a small control group, dose adjustments 

during the study, high mortality in high-dose female rats, and lack of cholinesterase measurements, 

hematology, or clinical chemistry) render this study inappropriate for use in drawing conclusions 

regarding the carcinogenicity of methyl parathion. 

EPA (1988a) has discussed the results of another carcinogenicity bioassay on methyl parathion in rats. 

Results of this study have not been presented in a peer-reviewed scientific journal and are not available to 

the public. 

Genotoxicity. No reliable data in humans exist to indicate whether methyl parathion may act by a 

genotoxic mechanism. One study reported a temporary but significant increase in chromatid breaks and 

stable chromosomal aberrations in two subjects after ingestion of methyl parathion (Van Bao et al. 1974), 

but another study reported no significant differences in five subjects after ingestion of methyl parathion 

when compared with 15 controls (Czeizel 1994). A study that involved combined inhalation and dermal 

exposure of workers to methyl parathion showed no increase in chromosomal aberrations in their 
 

 

METHYL PARATHION 105 

3. HEALTH EFFECTS 

lymphocytes (De Cassia Stocco et al. 1982). The results of available in vivo studies in animals (Degraeve 

et al. 1985; Grover and Malhi 1985; Huang 1973; Mathew et al. 1992; Tripathy et al. 1987; Waters et al. 

1982) and the results of in vitro studies (Chen et al. 1981; Dean 1972; Degraeve et al. 1985; GomezArroyo et al. 1987; Griffin and Hill 1978; Huang 1973; Kumar et al. 1993; Mohn 1973; Rashid and 

Mumma 1984; Shigaeva and Savitskaya 1981; Sobti et al. 1982; Waters et al. 1982) are equivocal. 

Since in vivo tests in exposed human populations would involve concomitant exposure to other toxicants, 

it would be difficult to assess the genotoxic potential of methyl parathion alone. Therefore, additional 

well-designed in vitro studies using human cell lines are needed to determine the effects of methyl 

parathion on various genotoxic parameters (e.g., sister chromatid exchange, chromosomal aberrations, 

unscheduled DNA synthesis). 

Reproductive Toxicity. No information is available in humans to indicate that methyl parathion 

affects reproductive function. No information is available on the reproductive effects in animals of 

inhaled or dermally administered methyl parathion. The limited available data indicate that methyl 

parathion is not toxic to male germ cells of mice following oral exposure (Degraeve et al. 1985; Waters et 

al. 1982), except possibly at very high doses (Mathew et al. 1992; Pagulayan et al. 1994). Also, negative 

data exist for histopathological effects on the reproductive system of dogs following ingestion of methyl 

parathion in the diet (Suba 1981). Additional studies in animals are needed to fully assess the 

reproductive toxicity of methyl parathion. 

EPA (1988a) has discussed the results of two reproductive studies in rats. Results of these studies have 

not been presented in peer-reviewed scientific journals and are not available to the public. If these data 

become available, they will provide valuable information on the reproductive hazards of methyl 

parathion. 

Developmental Toxicity. No information is available in humans to indicate that methyl parathion 

affects development. Rapid (within 30 minutes to 1 hour) placental transfer of methyl parathion has been 

demonstrated in rats following oral (Ackermann and Engst 1970) and dermal (Abu-Qare et al. 2000) 

administration to the dams. Oral studies in rats indicate that methyl parathion can induce subtle 

behavioral alterations in offspring at doses that do not induce clinical signs of maternal toxicity and can 

reduce acetylcholinesterase activity in maternal and fetal brain (Crowder et al. 1980; Gupta et al. 1985). 

Oral administration of methyl parathion to rat dams only during gestation or gestation and lactation did 

not affect electrocorticograms and evoked potentials in their offspring at 12 weeks of age, but similar 
 

 

METHYL PARATHION 106 

3. HEALTH EFFECTS 

administration to the dams followed by direct administration to the offspring from weaning through 

12 weeks of age did affect these end points in a dose-related manner (Desi et al. 1998). Although these 

studies indicate that methyl parathion may be a developmental neurotoxicant, all three studies have 

limitations of experimental design or reporting. No NOAEL was identified for the neurobehavioral 

effects and the dosing regimens were inadequate to demonstrate a dose response. The reporting of 

experimental design and results lacked detail in the electrophysiological study. A well-designed 

developmental neurotoxicity study is needed to confirm and extend these observations, and to define the 

dose-response and critical periods for neurotoxicity. There is some evidence of neurotoxicity in adult 

humans and animals from inhalation and dermal toxicity. If methyl parathion is confirmed as a 

developmental neurotoxicant by the oral route, it would likely be a developmental neurotoxicant by these 

routes as well. Further testing would be needed to confirm this. 

Immunotoxicity. Only a single case report of skin allergy to methyl parathion has been reported in 

humans (Lisi et al. 1987). No studies are available in humans exposed to methyl parathion via the 

inhalation or oral route. Based on limited animal studies, immunotoxicity may be a sensitive end point of 

methyl parathion-induced toxicity (Shtenberg and Dzhunusova 1968; Street and Sharma 1975). Thus, 

humans may be at risk for adverse immunological effects following exposure to methyl parathion. The 

limited information available on the effects of combined exposure to methyl parathion suggest the its 

toxicity is not route-dependent. Therefore, there is no reason to suspect that the immunotoxic effects 

observed following oral exposure of animals are route-specific. 

Some animal studies indicate that dietary exposure to methyl parathion causes decreased humoral and 

cellular responses (Shtenberg and Dzhunusova 1968; Street and Sharma 1975). A more recent, welldesigned animal study that included a battery of immuno/lymphoreticular end points showed few effects 

at the nonneurotoxic doses tested (Crittenden et al. 1998). No adequate studies are available in humans to 

assess the immunotoxic potential of methyl parathion. Therefore, studies measuring specific immunologic parameters in occupationally exposed populations are needed to provide useful information. Further 

studies are also needed to investigate the mechanism for methyl parathion-induced immunotoxicity since 

this information would help to identify special populations at risk for such effects. 

Neurotoxicity. Information in both humans and animals indicates that the nervous system is the major 

target of methyl parathion-induced toxicity following acute exposure by any route (Daly 1989; Dean et al. 

1984; EPA 1978e; Fazekas 1971; Gupta et al. 1985; Nemec et al. 1968; Roberts et al. 1988; Suba 1984; 

Yamamoto et al. 1982; Youssef et al. 1987). The most prominent signs of acute exposure to methyl 
 

 

METHYL PARATHION 107 

3. HEALTH EFFECTS 

parathion in humans via the oral and concomitant inhalation and dermal exposure routes are lethargy, 

nausea, vomiting, increased respiratory secretion, muscle fasciculations, and miosis (Dean et al. 1984). In 

rodents, oral exposure to methyl parathion causes convulsions, ataxia, abnormal gait, tremors, and 

behavioral impairment in offspring (EPA 1978e; Gupta et al. 1985; Miyamoto et al. 1963b; Suba 1984). 

Since the information available on the neurotoxic effects of methyl parathion indicates that the chemical 

behaves similarly across routes of exposure (Dean et al. 1984; EPA 1978e; Skinner and Kilgore 1982a, 

1982b), it is unlikely that the neurotoxic effects observed following oral exposure are route-specific. 

Neuropsychiatric disturbances have been seen in humans who had long-term exposure to high levels of 

organophosphates (Gershon and Shaw 1961); one case was associated with methyl parathion (Dille and 

Smith 1964). Moreover, the injection of methyl parathion into animals resulted in changes in brain 

components, such as increases in lipid content of the brain (Hasan and Khan 1985). Reliable information 

is lacking in humans on potential neurological effects of long-term, low-level exposure to methyl 

parathion as well as on potential long-term effects of acute high exposure to methyl parathion. This 

information can only be obtained from evaluation of cohorts exposed exclusively to methyl parathion, but 

data from subjects exposed to more than one organophosphate would still be helpful. 

Epidemiological and Human Dosimetry Studies. The vast majority of reviewed literature 

concerning the health effects of methyl parathion in humans described case reports of occupational 

exposure or accidental or intentional ingestion of methyl parathion (Dean et al. 1984; Fazekas 1971; 

Fazekas and Rengei 1964; Rider et al. 1969; Rodnitzky et al. 1978). No epidemiological studies are 

available. The information on human exposure is limited because of the possible concurrent exposure to 

other chemicals, and the duration and the level of exposure to methyl parathion cannot be quantified from 

the information presented in these reports. Differences in formulation can also be a confounding factor. 

The most likely identifiable subpopulations exposed to methyl parathion are pesticide applicators, farm 

workers, individuals involved in the production of methyl parathion, or individuals exposed in recently 

and illegally sprayed homes or offices. Well-designed epidemiological studies of these exposed workers 

are needed. Specific assessments of cancer risks and examination of the effects of methyl parathion on 

the nervous, hematological, and immune systems would be important since these appear to be the major 

end points of toxicity in experimental animals. If methyl parathion causes adverse effects in any of these 

target organs or systems, then these human end points can be used to monitor methyl parathion exposure 

in individuals living near hazardous waste sites or in recently and illegally sprayed homes or offices. 

Biomarkers of Exposure and Effect. 
 

METHYL PARATHION 108 

3. HEALTH EFFECTS 

Exposure. Data are available on biomarkers of exposure of methyl parathion in humans and experimental 

animals. The data on the persistence of methyl parathion and its metabolites indicate that they are not 

reliable indicators for assessing long-term, low-level exposure (Abu-Qare et al. 2000; Dean et al. 1984; 

EPA 1978e; Fazekas 1971; Morgan et al. 1977; Ware et al. 1975) largely because methyl parathion is 

extensively metabolized and the metabolites are rapidly eliminated. Short-term (<1 day) biomarkers are 

total urinary 4-nitrophenol and alkyl phosphates (Morgan et al. 1977); these biomarkers are nonspecific. 

Blood methyl parathion is also a short-term biomarker (Abu-Qare et al. 2000; Ware et al. 1975) and is 

specific. Additional studies of the general population correlating methyl parathion metabolite levels with 

health status as well as with dietary habits would provide useful information for risk characterization and 

risk assessment. 

Effect. There are no biomarkers of effects specific for methyl parathion. As an organophosphate 

pesticide, methyl parathion, in sufficient amounts, produces typical signs and symptoms of cholinergic 

stimulation. Plasma and RBC cholinesterase activities are widely used as biomarkers of exposure and 

effect for organophosphates, but alone, their levels do not predict whether adverse health effects will 

occur except in cases of significant inhibition. Data are available on cholinesterase levels in humans and 

animals following exposure to methyl parathion (Midtling et al. 1985; NIOSH 1976; Tafuri and Roberts 

1987). Because baseline data for plasma and erythrocyte cholinesterase are not usually available for 

nonoccupationally exposed individuals, additional studies of normal values by age and sex are needed for 

assessing potential adverse effects. As mentioned under biomarkers of exposure, additional studies of the 

general population correlating methyl parathion metabolite levels with health status and dietary habits 

would be useful. 

Absorption, Distribution, Metabolism, and Excretion. Evidence of absorption comes from the 

occurrence of toxic effects following exposure to methyl parathion by all three routes (Fazekas 1971; 

Miyamoto et al. 1963b; Nemec et al. 1968; Skinner and Kilgore 1982b). These data indicate that the 

compound is absorbed by both humans and animals. No information is available to assess the relative 

rates and extent of absorption following inhalation and dermal exposure in humans or inhalation in 

animals. A dermal study in rats indicates that methyl parathion is rapidly absorbed through the skin 

(Abu-Qare et al. 2000). Additional data further indicate that methyl parathion is absorbed extensively and 

rapidly in humans and animals via oral and dermal routes of exposure (Braeckman et al. 1983; 

Hollingworth et al. 1967; Ware et al. 1973). However, additional toxicokinetic studies are needed to 

elucidate or further examine the efficiency and kinetics of absorption by all three exposure routes. 
METHYL PARATHION 109 

3. HEALTH EFFECTS 

Limited information from case reports is available regarding the distribution of methyl parathion in 

humans following dermal exposure with possible concomitant inhalation exposure (Ware et al. 1973, 

1974, 1975). Following accidental oral or inhalation exposure to methyl parathion, clinical signs and 

symptoms or histopathological findings indicated that the compound was distributed to various tissues 

(Dean et al. 1984; Fazekas 1971; Fazekas and Rengei 1964). Although no quantitative information is 

available on the rate and extent of methyl parathion distribution in animals, the qualitative information for 

oral exposure does provide evidence as to the most likely target organs following both short- and longterm exposure (Galal et al. 1975; Gupta et al. 1985; Miyamoto et al. 1963b; Shtenberg and Dzhunusova 

1968; Sonnenschein et al. 1989a, 1989b; Street and Sharma 1975; Williams et al. 1959). Only limited 

data exist for the distribution of methyl parathion in humans following dermal exposure. Information 

regarding distribution in animals following dermal exposure is available, but quantitative data may have 

been compromised since some degree of oral exposure may have also occurred (Abu-Qare et al. 2000). 

Therefore, additional data in animal studies are needed to determine the distribution and half-life in 

various tissues following inhalation, oral, dermal, and intravenous exposure. 

The available information in humans regarding the metabolism of methyl parathion is limited to in vitro 

studies (Hollingworth et al. 1973). However, the in vitro (Benke and Murphy 1975; Benke et al. 1974; 

Hollingworth et al. 1973; Nakatsugawa et al. 1968; Neal and DuBois 1965) metabolic pathway of this 

chemical has been characterized in animals. 

No studies were located regarding excretion of methyl parathion in humans following inhalation 

exposure. The limited information available from human case studies indicates that the chemical's 

metabolites are rapidly excreted primarily in the urine in humans following oral (Morgan et al. 1977) or 

dermal (Ware et al. 1974, 1975) exposure and in animals following oral (Hollingworth et al. 1973) or 

dermal (Abu-Qare et al. 2000) exposure. 

Practically all toxicokinetic properties reported are based on the results from acute exposure studies. 

Generally, no information was available regarding intermediate or chronic exposure to methyl parathion. 

Because methyl parathion is an enzyme inhibitor, the kinetics of metabolism during chronic exposure 

could differ from those seen during acute exposure. Similarly, excretion kinetics may differ with time. 

Thus, additional studies on the distribution, metabolism, and excretion of methyl parathion and its toxic 

metabolite, methyl paraoxon, during intermediate and chronic exposure are needed to assess the potential 

for toxicity following longer-duration exposures. 
 

 

 

METHYL PARATHION 110 

3. HEALTH EFFECTS 

Comparative Toxicokinetics. The data available on the toxicity of methyl parathion in humans are 

from acute exposure where neurotoxicity is the end point of concern (Dean et al. 1984; Fazekas 1971). 

This effect is also seen in animals after acute exposure (EPA 1978e; Miyamoto et al. 1963b; Yamamoto et 

al. 1982; Youssef et al. 1987). In addition, hepatic and gastrointestinal effects have also been observed in 

humans (Fazekas 1971; Fazekas and Rengei 1964) and animals (NCI 1979; Sonnenschein 1989a, 1989b). 

It is unclear whether these effects are primary or secondary. No toxicokinetic studies have been 

performed in humans, and information on the rate and extent of absorption, distribution, half-life in 

various animal tissues, and excretion is primarily limited to a single dermal study in a single animal 

species (Abu-Qare et al. 2000). Additional studies on the comparative toxicokinetics of both methyl 

parathion and methyl paraoxon by various routes of exposure are needed to resolve uncertainty associated 

in assessing the health risks. 

Methods of Reducing Toxic Effects. There is good information on the procedures used to limit 

absorption and to interfere with the mechanism of action of methyl parathion after acute exposures 

(Aaron and Howland 1998; Bronstein and Currance 1988; EPA 1989b; Proctor et al. 1988; Stutz and 

Janusz 1988). However, no information is available on dealing with long-term, low-level exposures. 

This may be due, in part, to the limited information on toxic effects associated with such exposures. If 

additional information becomes available indicating adverse health effects of long-term exposures, then 

studies examining methods for mitigating the effects of such exposures would become a data need. 

Children’s Susceptibility. Present information indicates a potential for age-related differences in 

susceptibility to methyl parathion. However, data are limited in both human and animal studies. In future 

incidents involving methyl parathion poisoning of both children and adults, better estimates should be 

made on exposure levels, exposure routes, and urinary metabolite levels relative to the observed 

symptoms of toxicity. Additional animal studies are needed to further investigate the effects of methyl 

parathion on developing nervous systems. Other studies could compare neurological effects in immature 

animals of various ages with those seen in adults, particularly via the oral or inhalation exposure routes. 

Specific data needs relating to both pre- and postnatal exposures and development are discussed above 

under Developmental Toxicity. Furthermore, metabolic pathways and enzymatic activity for methyl 

parathion should be more clearly elucidated since potential age-related differences in the ability to 

metabolize methyl parathion could result in age-related differences in toxicity; suggestive evidence of 

age-related differences in metabolism was reported in rats (Benke and Murphy 1975). Biomarkers of 

exposure need to be further studied in order to better estimate human exposure at all age levels following 

acute or chronic exposure to methyl parathion. No information was located regarding pediatric-specific 
METHYL PARATHION 111 

3. HEALTH EFFECTS 

methods for reducing peak absorption following exposure to methyl parathion or reducing body burden. 

The information available indicates that methods to reduce peak absorption of methyl parathion and to 

interfere with the mechanism of action used for intoxication in adults are applicable to children. 

Developmental studies in animals are needed to quantitatively measure placental transfer of methyl 

parathion, to determine whether methyl parathion can be metabolized by placental tissue, and to further 

evaluate the transfer of methyl parathion and its metabolites to breast milk. 

Child health data needs relating to exposure are discussed in 6.8.1 Identification of Data Needs: 

Exposures of Children. 

3.12.3 Ongoing Studies 

A study of the dermal toxicokinetics of methyl parathion in female rats, sponsored by ATSDR, is being 

conducted at the University of Mississippi Medical Center. The principal investigator is Dr. Ing K. Ho, 

Department of Pharmacology and Toxicology, 500 North State Street, Jackson, Mississippi 39216-4505. 

ATSDR is conducting a health study to investigate the lasting health effects of methyl parathion exposure 

on children. In this study, ATSDR will be testing children in two states, Ohio and Mississippi. The 

principal Investigator is Dr. Rubina Imtiaz, ATSDR Division of Health Studies, 1600 Clifton Road, 

Atlanta, Georgia 30333. 

METHYL PARATHION 113 

4. CHEMICAL AND PHYSICAL INFORMATION 

4.1 CHEMICAL IDENTITY 

The chemical identity of methyl parathion is shown in Table 4-1. 

4.2 PHYSICAL AND CHEMICAL PROPERTIES 

The physical and chemical properties of methyl parathion are summarized in Table 4-2. 
METHYL PARATHION 

4. CHEMICAL AND PHYSICAL INFORMATION 

114 

Characteristic 

Table 4-1. Chemical Identity of Methyl Parathion 

Value Reference 

Chemical name 

Synonyms 

Trade names 

Manufacture trade names 

Formulators’ trade names 

Discontinued names 

Chemical formula 

Chemical structure 

Identification numbers: 

CAS registry 

NIOSH RTECS 

EPA hazardous waste 

OHM/TADS 

DOT/UN/NA/IMCO 

shipping 

HSDB
 

NCI
 

Methyl parathion 

Dimethyl 4-nitrophenyl phosphorothioate; dimethyl 

p-nitrophenyl phosphorothioate; dimethyl p-nitrophenyl 

thiophosphate; dimethyl parathion; O,O-dimethyl 

O-(p-nitrophenyl) phosphorothioate 

A-Gro; Metaphos; Bay 11405; Bladan-M; 

Cekumethion; Dalf; Devithion; Drexel Methyl 

Parathion 4E; ENT 17,292; Floidal M; Gearphos; 

M40 & 80; ME-Parathion 

Paratox; Bladan; Metacide; Morphos; Frog; Parataf; 

Romethyl-P; Prompt; Sweeper; Fortune-P1; Silmepar; 

Metpar; Paramet; Foxy 

Amithion; Agrodol; Paration Metilico 500 or 720; AgroParathion; Vitamethion; Cekmethion; Devithion; 

Dhanudol; Penncap-M; Bration; Methion; Kikdot; 

Parathol; Woprophos-M; Parasul; Gearphos; Kilex 

Parathion; Metaphos; Patron M; Tekwaisa 

Paraton; Wofatox; Veto; Fosferna M50; Nitrox 80; 

Parapest M050; Sytemp 

C8H10NO5PS 

S 

CH3O P O NO2 

CH3O 

298-00-0 

TG0175000 

P071 

7216537 

Methyl parathion, liquid (DOT); Methyl parathion 

mixture, dry (DOT); methyl parathion, solid (DOT); 

UN 3017; organophosphorus pesticides, liquid, toxic, 

flammable, not otherwise specified 

NA 2783 (DOT) 

1168 

NCI-C02971 

Budavari 1989 

HSDB 1999 

IARC 1983; 

NPIRS 1986; 

RTECS 1989 

Meister et al. 1999 

Meister et al. 1999 

Meister et al. 1999 

Budavari 1989 

Budavari 1989 

HSDB 1999 

HSDB 1999 

HSDB 1999 

HSDB 1999 

HSDB 1999; 

RTECS 1989 

HSDB 1999 

RTECS 1989 

HSDB 1999 

CAS = Chemical Abstracts Services; DOT/UN/NA/IMCO = Department of Transportation/United Nations/North 

America/International Maritime Dangerous Goods Code; EPA = Environmental Protection Agency; 

HSDB = Hazardous Substances Data Bank; NCI = National Cancer Institute; NIOSH = National Institute for 

Occupational Safety and Health; OHM/TADS = Oil and Hazardous Materials/Technical Assistance Data Systems; 

RTECS = Registry of Toxic Effects of Chemical Substances 
METHYL PARATHION 115 

4. CHEMICAL AND PHYSICAL INFORMATION 

Table 4-2. Physical and Chemical Properties of Methyl Parathion 

Property Information Reference 

Molecular weight 263.23 Budavari 1989 

Color White solid (pure) or brownish liquid (technical) Weiss 1986 

Physical state Solid (crystals from cold methanol) Budavari 1989 

Solid Weiss 1986 

Melting point 37–38 EC Budavari 1989 

Boiling point 154 EC at 136 Pa HSDB 1999 

Decomposes above ambient temperature 

Decomposes violently at 120 EC Keith and Walters 1985 

Density at 20 EC 1.358 g/mL Budavari 1989 

Odor Characteristic, like rotten eggs or garlic Keith and Walters 1985; 

Weiss 1986 

Odor threshold: 

Water No data 

Air 0.012 ppm Ruth 1986 

Solubility: 

Water at 25 EC 50 ppm Budavari 1989 

Organic solvents Soluble in ethanol, chloroform, and aromatic Sunshine 1969 

and aliphatic solvents 

$10 mg/mL (at 23 EC) in DMSO and ethanol; Keith and Walters 1985 

very soluble in acetone 

Sparingly soluble in petroleum ether and some Tomlin 1994 

types of mineral oil 

Partition coefficients: 

Log octanol/water (Kow) 2.86 Hansch et al. 1995 

Log Koc 2.7 EPA 1980c 

Vapor pressure at 20 EC 9.7x10-6 mm Hg Keith and Walters 1985 

Henry’s law constant 6.2x10-6 atm m3

/mol Sanders and Seiber 1983 

4.4x10-7 atm m3

/mol Mackay and Shiu 1981 

Autoignition temperature No data 

Flashpoint 31.9 EC (open cup) NFPA 1986 

Flammability limits No data 

Conversion factors 1 ppm = 10.8 mg/m3 

Explosive limits May develop sufficient internal pressure at NFPA 1986 

ambient temperature to cause a container to 

rupture violently 

Explosion risk when heated Hawley 1987 

DMSO = dimethylsulfoxide 

METHYL PARATHION 117 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL 

5.1 PRODUCTION 

Methyl parathion is an organophosphorus insecticide that is commercially produced in the United States 

and abroad. Methyl parathion, O,O-dimethyl O-(4-nitrophenyl) phosphorothioate, is not known to occur 

as a natural substance (IARC 1983). It is commercially produced by the reaction of O,O-dimethyl phosphorochloridothionate and the sodium salt of 4-nitrophenol in acetone solvent (EPA 1974b; HSDB 1999; 

NIOSH 1976; NRC 1977; Worthing 1979). 

Methyl parathion was first commercially produced in the United States in 1952 (U.S. Tariff Commission 

1953) and was registered as an organophosphate insecticide in 1954 (NPIRS 1986). Production volume 

data are not available for the 1950s and 1960s and are sporadically available for the 1970s. In 1973, 

domestic production of methyl parathion was approximately 23.2 million kg (NRC 1977), while in 1975, 

it had increased to 24.4 million kg (USITC 1977a). A significant decline in production of methyl 

parathion occurred in 1977; the production levels dropped by 5.6 million kg from 1975 levels to 

18 million kg (USITC 1979). Production volume statistics for methyl parathion are not listed separately 

after 1977. In 1983, the combined domestic production capacity of methyl parathion and parathion was 

estimated at 29 million kg (IARC 1983). In the same year, production in western Europe was estimated 

in the range of 10–15 million kg annually (IARC 1983). No recent production data are available. 

Methyl parathion is produced or formulated in the United States by Cheminova Agro A/S, Griffin 

Corporation, and Elf Atochem North America (EPA 1999c). A summary of all of the manufacturers of 

methyl parathion in the United States was not located. Monsanto Co. and Kerr-McGee Chemical Corp. 

were the major producers for the period 1972 through 1988 (USITC 1973, 1975, 1977b, 1979, 1981, 

1982, 1983, 1984, 1985, 1986a, 1986b, 1987, 1989). Table 5-1 provides the production year, number of 

facilities, and the state of their location for each known domestic producer or formulator required to 

report Toxics Release Inventory (TRI) data to satisfy EPA requirements. TRI data are available for this 

chemical because it is on the list of chemicals for which annual releases are required to be reported to the 

EPA. 

Methyl parathion is marketed as a technical grade solution (80% methyl parathion) or in emulsifiable 

concentrate, wettable powder, ultra-low volume (ULV) liquid, dustable powder, and encapsulated 

suspension forms (HSDB 1999). The technical grade solution contains 80% active ingredient, 16.7% 
METHYL PARATHION 118 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL 

Table 5-1. Facilities that Produce, Process, or Use Methyl Parathion 

Number of Minimum amount on site Maximum amount on site Activities 

Statea facilities in poundsb in poundsb and usesc 

GA 1 1,000,000 9,999,999 8
 

MS 1 10,000 99,999 8
 

TX 1 10,000 99,999 13
 

Source: TRI99 2001 

a

Post office state abbreviations used 

b

Amounts on site reported by facilities in each state c

Activities/Uses: 

1. Produce 6. Impurity 10. Repackaging 

2. Import 7. Reactant 11. Chemical Processing Aid 

3. Onsite use/processing 8. Formulation Component 12. Manufacturing Aid 

4. Sale/Distribution 9. Article Component 13. Ancillary/Other Uses 

5. Byproduct 
METHYL PARATHION 119 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL 

xylene, and 3.3% inert ingredients. Stabilized methyl parathion solution is also available and contains 

80.0% active ingredient, 14.8% xylene, and 5.3% inert ingredients (IARC 1983). Methyl parathion is 

formulated and sold in mixtures with parathion (ethyl), malathion, and endosulfan (Berg 1981; EPA 

1999c). There are over 50 trade names for formulations and preparations of methyl parathion, including 

Methaphos, Gearphos, Cekumethion, and Devithion (IARC 1983; Meister et al. 1999; NPIRS 1986). 

5.2 IMPORT/EXPORT 

In 1971, 3 million kg of methyl parathion were imported into the United States (U.S. Tariff Commission 

1972). There was a decline in imports in the mid-1970s with levels of 499,000 kg in 1972 and only 

40,000 kg in 1975 (HSDB 1999). By 1980, this downward trend had reversed, and imports of methyl 

parathion were up to 413,000 kg (USITC 1981). 

In 1972, 5.68 million kg of methyl parathion were exported from the United States (HSDB 1999). 

Exports dropped to 3.01 million kg in 1984 (Bureau of the Census 1984). However, in 1985, exports 

increased to 4.14 million kg (Bureau of the Census 1986). No recent import/export data addressing 

methyl parathion are available. 

5.3 USE 

Methyl parathion is a broad-spectrum, nonsystemic, contact and stomach insecticide with some 

respiratory action used to control insects on a wide variety of crops (HSDB 1999; Tomlin 1994). Methyl 

parathion controls a wide variety of insects including plant lice, thrips, aphids, and boll weevils 

(International Labour Office 1983; Meister 1988; NPIRS 1986; Weir and Hazleton 1981). Methyl 

parathion has also been used to control mites and tadpole shrimp (NPIRS 1986). Methyl parathion has 

been applied to cotton, field vegetables, rice, fruit trees, soybeans, alfalfa, nut crops, tobacco, 

ornamentals, forest trees, aquatic food crops, and mosquito breeding sites (IARC 1983; NPIRS 1986; 

Spencer 1982). Methyl parathion is generally applied to the leaves or the aerial portion of the crop using 

either aircraft or ground spray equipment (NPIRS 1986). 

Because of its very high acute toxicity, methyl parathion is a restricted-use pesticide (EPA 1985b). In the 

United States, methyl parathion formulations must be used under the direct supervision of a certified 

pesticide applicator (EPA 1980b). The certified pesticide applicator must be physically present during 

mixing, loading, application, equipment repair, and equipment cleaning (NPIRS 1986). Originally, no 
METHYL PARATHION 120 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL 

worker was allowed to enter a field treated with methyl parathion <48 hours after the treatment (EPA 

1980b); that interval has been increased to 4–5 days (EPA 1999d). EPA has canceled many of the food 

crop uses of methyl parathion, including fruits and vegetables commonly eaten by children, some other 

vegetable uses, some feed uses, and all nonfood uses such ornamental plants and nursery stock uses. This 

action was taken because of a concern for risks to children and to workers. Some food and feed uses are 

to be maintained (EPA 1999d, 1999e). 

Data related to the domestic use of methyl parathion by volume for the years 1973–1984 show that use of 

methyl parathion was estimated to be 18.1 million kg in 1973 (NRC 1977) and 21.8 million kg in 1974 

(USDA 1978). In 1976, only 10.4 million kg of methyl parathion were used by U.S. farmers on major 

crops; however, this represents 17.5% of the total quantity of all active insecticide ingredients used on 

those crops in 1976 (USDA 1978). In 1978, total usage of methyl parathion is estimated to have been 

11.3 million kg; of this amount, an estimated 9.7 million kg of methyl parathion were used on cotton 

(USDA 1978). The reduction in use from 1974 to 1978 is generally attributed to the development of 

resistant insect strains and the use of integrated pest management practices (USDA 1978). The use of 

methyl parathion as a substitute for DDT in the late 1970s and early 1980s served to increase usage and 

reverse this downward trend (Butler et al. 1981b). The amount of methyl parathion used in the United 

States in 1989 was estimated to be 7.65 million pounds active ingredient/year (HSDB 1999). For the 

period 1987–1997, the annual amount used was 4.2 million pounds of methyl parathion per 5 million 

acres treated (EPA 1999c). 

Data collected from federal and state pesticide surveys of insecticide use (Giannessi and Anderson 1995) 

show the following crops were treated with methyl parathion in the United States during the 1992 crop 

year: alfalfa, apples, artichokes, barley, broccoli, brussel sprouts, cabbage, cantaloupes, carrots, 

cauliflower, celery, cherries, collards, corn, cotton, dry bean, dry peas, grapes, green beans, green peas, 

lettuce, nectarines, oats, onions, other hay, peaches, pears, pecans, potatoes, rice, soybeans, spinach, 

strawberries, sugarbeets, sunflowers, sweet corn, sweet peppers, tomatoes, watermelons, and wheat. 

Table 5-2 shows the total number of pounds per acre of methyl parathion that were applied to crops in 

each state in 1992. 
METHYL PARATHION 121 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL 

Table 5-2. Methyl Parathion Use in Crop Production in 1992 

State Pounds active ingredient/acre/year 

Alabama 365,640 

Arizona 87,203 

Arkansas 237,731 

California 85,432 

Colorado 12,682 

Connecticut 1,449 

Delaware 21,125 

Florida 19,939 

Georgia 75,576 

Idaho 14,893 

Illinois 101,443 

Indiana 17,390 

Iowa 5,927 

Kansas 201,749 

Kentucky 8,700 

Louisiana 889,789 

Maryland 6,654 

Massachusetts 1,264 

Michigan 61,118 

Minnesota 21,080 

Mississippi 1,818,501 

Missouri 50,311 

Montana 31,341 

Nebraska 507,880 

New Jersey 7,101 

New Mexico 6,146 

New York 28,018 

North Carolina 5,227 

North Dakota 163,620 

Ohio 1,984 

Oklahoma 484,960 

Oregon 12,266 

Pennsylvania 14,758 
METHYL PARATHION 122 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL 

Table 5-2. Methyl Parathion Use in Crop Production in 1992 (continued) 

State Pounds active ingredient/acre/year 

Rhode Island 178 

South Carolina 83,670 

South Dakota 12,540 

Tennessee 3,850 

Texas 274,446 

Utah 5,328 

Virginia 19,972 

Washington 115,689 

West Virginia 11,337 

Wisconsin 59,485 

Wyoming 169 
METHYL PARATHION 123 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL 

5.4 DISPOSAL 

In 1974, EPA recommended the incineration of methyl parathion at organic pesticide incinerators. If 

appropriate incineration facilities were not available, then open field burial at designated landfills was 

permitted (EPA 1974a). EPA also recommended that combustible containers used for methyl parathion 

be disposed of in pesticide incinerators or in designated landfills. Noncombustible containers should first 

be triple rinsed and, if in good condition, returned to the manufacturer or a drum reconditioner for reuse 

with methyl parathion. Noncombustible containers that are not to be reused should be punctured and 

transported to a scrap metal facility for recycling or buried in a designated landfill site (EPA 1974a). 

In 1980, methyl parathion waste became subject to the Resource Conservation and Recovery Act 

(RCRA). According to RCRA, when methyl parathion becomes a waste (e.g., as an off-specification 

batch produced by a manufacturer) it must be managed as a hazardous waste according to federal and/or 

state regulations. Any containers used to hold this waste must also be managed as a hazardous waste 

(EPA 1980a). The RCRA hazardous waste code for methyl parathion is P071. When there is an 

accidental release of methyl parathion, the Comprehensive Environmental Response, Compensation, and 

Liability Act (CERCLA) reportable quantity is 45.4 kg or 100 pounds (EPA 1985f). Methyl parathion is 

on the list of chemicals for which annual releases to the environment must be reported to the TRI as 

established by the EPA (EPA 1999c). 

Improved methods for the disposal of methyl parathion are being considered. In 1981, methyl parathion 

was considered as a potential candidate for rotary kiln incineration and fluidized bed incineration 

(EPA 1981b). An accelerated degradation process for methyl parathion, which involved reducing the 

compound in soil with acid and zinc to its less toxic degradates, was found to be effective (Butler et 

al. 1981b). No recent information on disposal is available. 

Effluent containing methyl parathion may not be discharged into lakes, streams, ponds, estuaries, oceans, 

or public waters unless the compound is specifically identified in a National Pollutant Discharge 

Elimination System (NPDES) permit. Moreover, discharge of effluent that contains methyl parathion is 

forbidden without prior notice to the sewage treatment plant authority (NPIRS 1986). 

METHYL PARATHION 125 

6. POTENTIAL FOR HUMAN EXPOSURE 

6.1 OVERVIEW 

Methyl parathion is a broad-spectrum agricultural insecticide that is released to the environment primarily 

through spraying of the insecticide on a variety of agricultural products. Once methyl parathion is 

introduced to the environment, it is degraded by hydrolysis, photolysis, or by biodegradation from 

microorganisms found in most sediment, soils, and water. Methyl parathion is primarily confined to the 

application area, but some can be transported by rain, fog, and wind to other areas. Methyl parathion 

adsorbs to the soil and is relatively immobile. As a result, leaching into groundwater is not usually 

observed. Volatilization has been observed to occur from plants and soil postapplication, with 

volatilization from plants being the faster of the two. Limited studies show that bioconcentration of 

methyl parathion does not occur to a significant extent and that what is accumulated in plants and animals 

is rapidly metabolized. Methyl parathion is not widely dispersed or persistent in the environment. 

Residue amounts of methyl parathion have been detected in air, water, fish, soil, and agricultural crops 

consumed as foods. 

Methyl parathion is approved by the EPA only for use on agricultural crops. As a result, the general 

population is not likely to be exposed to large amounts of methyl parathion. Some exposure to residues 

of methyl parathion is possible, however, as many studies show that methyl parathion has been detected 

in foods and atmosphere samples. Populations living within or very near areas of heavy methyl parathion 

use would have an increased risk of exposure to large amounts of methyl parathion through dermal 

contact with contaminated plants, by inhalation of the mist formed from the applied insecticide, or by 

ingestion of water or food-borne residues. Those likely to receive the highest levels of exposure are those 

who are involved in the production, formulation, handling, and application of methyl parathion. Dermal 

contact appears to be the major route of exposure, while inhalation may also be an important route of 

exposure for those working in these operations. 

Methyl parathion has been identified in at least 16 of the 1,585 hazardous waste sites that have been 

proposed for inclusion on the EPA National Priorities List (NPL) (HazDat 2001). However, the number 

of sites evaluated for methyl parathion is not known. The frequency of these sites can be seen in 

Figure 6-1. 
Figure 6-1. Frequency of NPL Sites with Methyl Parathion Contamination 

1 2 4 

Frequency of

NPL Sites 

Derived from HazDat 2001 
METHYL PARATHION 127 

6. POTENTIAL FOR HUMAN EXPOSURE 

6.2 RELEASES TO THE ENVIRONMENT 

Methyl parathion has been released to the environment mainly as a result of its use as an insecticide on 

crops. It is applied to agricultural crops by aerial or ground spraying equipment. Methyl parathion has 

been detected in surface waters and sediments, rainwater, aquatic organisms, and food. There are no 

known natural sources of the compound. Methyl parathion has been identified in at least 16 of the 

1,585 hazardous waste sites on the NPL (HazDat 2001). 

According to recent Toxics Release Inventory (TRI) data, methyl parathion was discharged to air from 

two processing sites in the United States in 1999 (TRI99 2001). No releases to soil or water were 

reported. The TRI data should be used with caution because only certain facilities are require to report. 

This is not an exhaustive list. 

6.2.1 Air 

As a result of its use as an insecticide on cotton, fruit trees, vegetables, and other crops, methyl parathion 

is released directly to the atmosphere during application. It is applied primarily by spraying from aircraft 

or ground equipment (NPIRS 1986). Aerial application of methyl parathion to agricultural fields releases 

the insecticide to the air. 

Methyl parathion may also be introduced into the air as a result of its volatilization from plant surfaces, 

and somewhat from soil, especially in the period just after application. Under simulated field conditions 

(20 EC; air velocity 1 meter/second; relative air humidity 40–60%), an emulsifiable concentrate 

formulation of methyl parathion was applied to bare soil and bean plants. After 24 hours, the amounts of 

methyl parathion that had volatilized from bare soil and bean plants were 5 and 64% of the applied 

amount, respectively (Rudel 1997). 

Releases to the atmosphere from production facilities and disposal sites have also been reported. Studies 

have shown that releases of methyl parathion to the atmosphere occur in the vicinity of pesticideproducing factories. At two predominately downwind sites located 1 mile from a plant producing methyl 

parathion, average monthly concentrations were <0.57 and <0.64 ng/m3

 (Foster 1974). Air emissions 

from methyl parathion production facilities have been reported to contain 1.0 kg/1,000 kg pesticide 

produced. In addition, evaporation from holding ponds for pesticide waste potentially contributes 

7.4 mg/1,000 kg pesticide produced to the atmosphere (EPA 1978d). 
METHYL PARATHION 128 

6. POTENTIAL FOR HUMAN EXPOSURE 

The most recent TRI data indicate that six sites in the United States processed methyl parathion in 1999 

(TRI99 2001). The total of reported releases to air was 15 pounds, representing 100% of all 

environmental releases (Table 6-1). The TRI data should be used with caution because only certain types 

of facilities are required to report. This is not an exhaustive list. 

No information was found on the occurrence of methyl parathion in air samples collected at NPL sites. 

6.2.2 Water 

Methyl parathion can be released to surface waters by storm runoff from sprayed fields; atmospheric 

deposition following aerial application (wet deposition from rain and fog water); waste water releases 

from formulation, manufacturing, or processing facilities; and spills. 

Methyl parathion has been detected in runoff water from a cotton field at a concentration of 15 ppb. A 

semi-empirical prediction formula used to predict maximum concentrations of pesticides in agricultural 

runoff water estimated methyl parathion concentrations could be as high as 40 ppb (Wauchope and 

Leonard 1980). Methyl parathion has been detected in fog water near sites of application (Schomburg et 

al. 1991) and in rainwater (Nations and Hallberg 1992), suggesting that methyl parathion can be released 

to surface waters by wet deposition, the process that occurs after airborne residues dissolve in water. 

Methyl parathion could be released to water through atmospheric deposition following aerial application, 

but no data are available for evaluating the importance of this route of surface water contamination. 

Methyl parathion can be released to surface water by the release of waste water containing pesticide 

residues. In one report, methyl parathion was detected in pre-, mid-, and posttreatment waste water from 

a methyl parathion production plant (EPA 1978e). 

Spills may represent the greatest point source release of methyl parathion to groundwater and surface 

water. An accidental spill caused by a warehouse fire in Nebraska released methyl parathion to a 

drainage ditch that emptied into the Missouri River (Kawahara et al. 1967). In another incident, 10 tons 

of methyl parathion spilled in the Mediterranean Sea near Egypt as a result of a collision between two 

ships (Badawy et al. 1984). 

The most recent TRI data indicate that no releases of methyl parathion to water for the six sites in the 

United States that processed methyl parathion in 1999 (TRI99 2001). The TRI data should be used with 

caution because only certain types of facilities are required to report. This is not an exhaustive list. 
Table 6-1. Releases to the Environment from Facilities that Produce, Process, or Use Met

Reported amounts released in pounds per yeara 

Number 

Stateb 

of facilities Airc Water 

Underground injection Land 

Total on-site released 

Total off-sreleasee 

AR 1 No data No data No data No data No data No da

GA 1 5 No data No data No data 5 No da

MS 1 10 0 No data No data 10 No da

NE 1 No data No data No data No data No data No da

TX 2 0 No data No data No data 0 No da

Total 6 15 0 0 0 15 

Source: TRI99 2001 aData in TRI are maximum amounts released by each facility.bPost office state abbreviations are used.cThe sum of fugitive and stack releases are included in releases to air by a given facility. dThe sum of all releases of the chemical to air, land, water, and underground injection wells. eTotal amount of chemical transferred off-site, including to publicly owned treatment works (POTW).
METHYL PARATHION 130 

6. POTENTIAL FOR HUMAN EXPOSURE 

Methyl parathion is listed in the HazDat database of chemicals detected in surface water or groundwater 

at NPL sites. 

6.2.3 Soil 

Most of the methyl parathion deposited onto soils is through deposition of spray droplets that fall to the 

ground following spraying. An estimated 5.95 million pounds of methyl parathion were used on a variety 

of crops in the United States in 1992 (Gianessi and Anderson 1995). 

Methyl parathion may also be released to soils by improper handling of pesticide formulations during 

processing or handling. In a sampling of soils collected from processing facilities in Illinois, methyl 

parathion was detected in soil at 2 of the 49 sites tested (Krapac et al. 1995). 

The most recent TRI data indicate that no releases to soil were reported for the six sites in the United 

States that processed methyl parathion in 1999 (TRI99 2001). The TRI data should be used with caution 

because only certain types of facilities are required to report. This is not an exhaustive list. 

Methyl parathion is listed in the HazDat database of chemicals detected in soils at NPL sites. 

6.3 ENVIRONMENTAL FATE 

The methyl parathion released to the atmosphere can be transported back to surface water and soil by wet 

deposition. Methyl parathion that is released to the atmosphere can also be transformed by indirect 

photolysis to its oxygen analog, methyl paraoxon, by oxidation with photochemically produced oxygen 

radicals. However, methyl parathion is not expected to undergo significant transformation to methyl 

paraoxon. 

In surface waters, methyl parathion degrades by biotransformation, hydrolysis, volatilization, and 

photolysis (EPA 1978c, 1981a). Biodegradation is expected to be the predominant degradation process. 

Adsorption to sediment and suspended matter may significantly affect the degradation processes (Lartiges 

and Garrigues 1995). 

In soil and sediments, methyl parathion adsorbs to soil and is expected to display moderate mobility (EPA 

1980c). The major degradation process of methyl parathion in soil is biodegradation by microbes 

(Badway and El-Dib 1984). Degradation by hydrolysis has been observed to occur at higher temperatures 
METHYL PARATHION 131 

6. POTENTIAL FOR HUMAN EXPOSURE 

(Sharmila et al. 1988). Little methyl parathion appears to volatilize from soil (EPA 1984a) or leach into 

groundwater (Albanis et al. 1988a, 1988b; Jury et al. 1983, 1987a, 1987b; McLean et al. 1988). 

6.3.1 Transport and Partitioning 

Data indicate that methyl parathion generally does not remain in the air for long periods or migrate far 

from the application site following aerial application when wind conditions are satisfactory. Studies 

following application of methyl parathion indicate that it is rapidly removed from the atmosphere 

(Jackson and Lewis 1978), probably by wet and dry deposition. Methyl parathion has been detected in 

the water phase of fog (Glotfelty et al. 1987; Sharmila et al. 1988), suggesting wet deposition processes. 

Its deposition has been found to be confined primarily to the intended application site with negligible 

exposure estimated to occur 100 yards from the center of the target field (Draper and Street 1981). Wind 

conditions, which would be expected to be a factor in methyl parathion transport in air, were negligible in 

this study. 

The vapor pressure of methyl parathion is relatively low (9.7x10-6 mmHg), as is the Henry's law constant 

(6.2x10-6 atm-m3

/mol) (EPA 1984a; HSDB 1999; Rice et al. 1997; Sanders and Seiber 1983). The 

volatilization of methyl parathion from soil and water has generally been found to be correspondingly 

low. 

Mathematical models have also predicted a low volatility for methyl parathion (Jury et al. 1983; McLean 

et al. 1988). One study using a laboratory model designed to mimic conditions at soil pit and evaporation 

pond disposal sites (Sanders and Seiber 1983) did find a high volatility from the soil pit model (75% of 

the deposited material), but a low volatility for the evaporation pond model (3.7% of the deposited 

material). A study of methyl parathion and the structurally similar compound ethyl parathion, which have 

similar vapor pressures, found that methyl parathion underwent less volatilization than ethyl parathion; in 

a review of the data, the reduced level of volatilization for methyl parathion was determined to be due to 

its adsorption to the soil phase (Álvarez-Benedi et al. 1999). 

Methyl parathion is only slightly soluble in pH 7 water (55–60 ppm). This affects its mobility in water 

and its ability to be leached or solubilized into the water phase of a soil-water system. Factors most likely 

to affect the adsorption of methyl parathion in soil are organic matter content and cation exchange 

capacity. In soils of low organic matter (e.g., subsurface soils), calcium concentration, which affects the 

hardness of the water, may also be important (Reddy and Gambrell 1987). Several studies have shown 
METHYL PARATHION 132 

6. POTENTIAL FOR HUMAN EXPOSURE 

that, in most cases, methyl parathion does not move very far from the soil surface following application 

(Albanis et al. 1988a, 1988b; Jury et al. 1983, 1987a; McLean et al. 1988). One reason for this limited 

mobility is that most of the methyl parathion may degrade before significant migration can occur. 

The solubility of methyl parathion is not sufficient to pose a problem in runoff water as determined by an 

empirical model of Wauchope and Leonard (1980). Some recent monitoring data, however, indicate that 

methyl parathion has been detected in surface waters (Senseman et al. 1997). In a study to determine the 

residue levels of pesticides in shallow groundwater of the United States, water samples from 1,012 wells 

and 22 springs were analyzed for methyl parathion. No methyl parathion was detected in any of the water 

samples (Kolpin et al. 1998). In a study of water from near-surface aquifers in the Midwest, no methyl 

parathion was detected in any of the water samples from 94 wells that were analyzed for pesticide levels 

(Kolpin et al. 1995). Leaching to groundwater does not appear to be a significant fate process. 

When the concentrations of methyl parathion in soil are high, such as those found at hazardous waste or 

spill sites, leaching may be a significant source of contamination (Albanis et al. 1988b; Jury et al. 1987a). 

Several authors have found soil adsorption isotherms to be linear at lower concentrations, but nonlinear at 

higher concentrations (EPA 1980c; Rao and Davidson 1979). This suggests that while methyl parathion 

may be relatively immobile in soil at the lower concentrations used in agriculture, it may be more mobile 

at the higher concentrations found at hazardous waste sites and spills. 

One of the most important factors affecting the mobility of methyl parathion in the environment is its 

strong adsorption to soils. One study showed that after a 49-day incubation, 54% of the initial applied 

methyl parathion remained in the soil (Gerstl and Helling 1985). Factors affecting the adsorption of 

methyl parathion are organic matter content of the soil and sediment, and the cation exchange capacity of 

the soil. Values for organic-carbon normalized soil adsorption coefficients, Koc, in five soil types were 

determined by EPA (1980c) and were found to average 496, equal to a log Koc of 2.7. Estimates of log 

Koc, calculated from the octanol-water coefficient (Kow), solubility, and melting point data ranged from 

2.93 to 3.47, and compared favorably with literature values (Karickhoff 1981). McLean et al. (1988) 

estimated a lower Koc of 39, equal to a log Koc of 1.59. More recently, a Koc of 5,100, equal to log Koc 3.7, 

has been reported (HSDB 1999). These Koc values indicate that methyl parathion is moderately mobile to 

immobile in soil (Swann et al. 1983). 

Estimates of bioconcentration factors, BCF, in aquatic organisms, based on calculations from water 

solubility and Koc, gave a log BCF of 1.80–2.89 (Kenaga 1980). Studies in outdoor ponds yielded log 
METHYL PARATHION 133 

6. POTENTIAL FOR HUMAN EXPOSURE 

BCF factors in fish ranging from 1.08 to 1.85, indicating that bioconcentration of methyl parathion is not 

an important fate process (Crossland and Bennett 1984). In another study, methyl parathion was added to 

the water of a carp-rearing pond and the concentration of methyl parathion was measured in water, soil, 

macrophytes, and carp over a 35-day period. Results showed that methyl parathion accumulated in 

macrophytes for 1 day and in carp for 3 days following exposure, and then dissipated. The concentrations 

of methyl parathion decreased in macrophytes by 94% by day 35 and by 98% in carp tissue by day 28 

(Sabharwal and Belsare 1986). These data indicate the potential for biomagnification in the food chain is 

likely to be low because methyl parathion appears to be metabolized in aquatic organisms. 

6.3.2 Transformation and Degradation 

6.3.2.1 Air 

Very little information exists in the literature on the transformation and degradation of methyl parathion 

in air. An early study indicated that direct photolysis of methyl parathion may occur; however, the 

products of this photolysis were not determined (Baker and Applegate 1974). A later study found a 

transformation product of methyl parathion, methyl paraoxon, in air samples taken from areas where 

methyl parathion had been applied. Formation of methyl paraoxon was attributed to the vapor phase 

oxidation of methyl parathion (Seiber et al. 1989). Recent monitoring studies in California have also 

found both methyl parathion and methyl paraoxon (Baker et al. 1996). 

6.3.2.2 Water 

Methyl parathion is rapidly degraded in natural water systems. The degradation of methyl parathion 

occurs much more rapidly in alkaline (pH 8.5) than in neutral (pH 7) or acidic (pH 5) conditions (Badawy 

and El-Dib 1984). A hydrolysis half-life of 72–89 days was calculated for fresh water at 25 EC and pH<8 

(EPA 1978c; Mabey and Mill 1978) compared with about 4 days at 40 EC and pH$8 (EPA 1978c). 

Under conditions typically encountered in the environment, with pHs between 5 and 9, methyl parathion 

is not expected to be a significant fate process. 

The degradation of methyl parathion by hydrolysis and biodegradation was studied in four types of water 

(ultrapure water, pH 6.1; river water, pH 7.3; filtered river water, pH 7.3; and seawater, pH 8.1) 

maintained at 6 and 22 EC, in the dark. The half-lives of methyl parathion at 6 EC in the four water types 

were determined to be 237, 95, 173, and 233 days, respectively, and the half-lives at 22 EC were 
METHYL PARATHION 134 

6. POTENTIAL FOR HUMAN EXPOSURE 

determined to be 46, 23, 18, and 30 days, respectively. The study shows that degradation rates increase 

with pH and temperature, and are fastest in river water (Lartiges and Garrigues 1995). 

Transformation and degradation of methyl parathion in water appear to be primarily biological 

(i.e., microbial), but chemical degradation (i.e., hydrolysis) may be important in some systems (EPA 

1978c, 1981a). In oligotrophic waters (i.e., low in microbial populations), hydrolysis is the major 

degradation mechanism (Baughman and Lassiter 1978; EPA 1978c, 1981a). The rate of chemical 

hydrolysis depends on pH and temperature. 

Studies in which methyl parathion is added to the water phase of sediment samples have detected no 

methyl parathion in the sediment, probably because the degradation rate exceeds the rate of deposition to 

the sediment (Crossland and Bennett 1984; EPA 1982b). This degradation appears to be primarily 

microbial. Experiments comparing the degradation of methyl parathion in tap water and natural pond 

water show similar rates of disappearance of methyl parathion. Loss rates increased in both water types 

when plants, sediment, or plants and sediment were added (Crossland and Bennett 1984). In experiments 

with seawater systems, seawater plus sediment contained only 3% of the applied methyl parathion after 

7 days, compared with 75% in seawater alone and 104% in sterile seawater (EPA 1981a). Degradation in 

water alone was also found to be significantly less than in water plus sediment in an estuarine system 

(Pritchard et al. 1987). Several studies in water systems have demonstrated that methyl parathion is 

rapidly degraded by the bacteria within aufwuchs communities (i.e., the microorganisms attached to 

plants, sediments, and mats) found in aquatic ecosystems (Crossland and Bennett 1984; Holm et al. 1983; 

Lewis and Holm 1981). Chemical/toxicity testing using natural river die-off water with sediment and a 

toxicity sensitive organism (mysid shrimp) demonstrated that methyl parathion degraded rapidly (half-life 

of 2.3 days) to nontoxic products (Cripe et al. 1987). 

In freshwater systems, the only biodegradation product detected was 4-nitrophenol, which was rapidly 

utilized and transformed to undetectable metabolites by the microorganisms present. In seawater, the 

main initial product was methyl aminoparathion, formed by reduction of the nitro group (Badawy and ElDib 1984). Studies in raw river water showed that 4-nitrophenol and dimethyl thiophosphoric acid are 

the main degradation products (Eichelberger and Lichtenberg 1971). 

Photolysis studies of methyl parathion have been reported. A study examining the photodegradation of 

methyl parathion in river and seawater at variable temperatures showed the half-lives to be 11 and 

34 days, respectively (Lartiges and Garrigues 1995). During photolysis in natural water 50% of the 
METHYL PARATHION 135 

6. POTENTIAL FOR HUMAN EXPOSURE 

original methyl parathion concentration was degraded in 8 days in the summer and 38 days in the winter 

(EPA 1978c). In a photolysis study of methyl parathion in fresh waters of Portugal, a half-life of 3 days 

in groundwater and a half-life of 4 days in river water were observed. The authors noted that the 

transformation products, which included methyl paraoxon, were more stable than the parent compounds 

studied (Castillo et al. 1997). 

6.3.2.3 Sediment and Soil 

In soils and sediments, microbial degradation and hydrolysis are important degradation processes. 

Studies have found that methyl parathion degrades more rapidly in anaerobic soil than in aerobic soils 

(Adhya et al. 1981, 1987; Brahmaprakash et al. 1987). An average half-life of 64 days was determined 

for nonflooded (aerobic) soils compared to an average half-life of 7 days in flooded (anaerobic) soils 

(Adhya et al. 1987). In experiments with 14C-labeled methyl parathion, 35% of the labeled compound 

was recovered from nonflooded soil after 28 days, compared with 9% recovered from flooded soil 

(Brahmaprakash et al. 1987). 

Results from other studies support the rapid degradation of methyl parathion in soils with a high water 

(i.e., low oxygen) content (Adhya et al. 1981, 1987; Brahmaprakash et al. 1987). Experiments in flooded 

and nonflooded soils showed that the redox potential affected both the rate of degradation and the 

transformation products of methyl parathion (Adhya et al. 1981, 1987). Transformation to volatile 

products was suggested by Brahmaprakash et al. (1987) as the reason that significant amounts of 14C from 

labeled methyl parathion could not be accounted for, especially in flooded soils. 

In a study of the degradation of methyl parathion in flooded (anaerobic), alluvial (pH 6.2) soil, samples 

were maintained at 6, 25, and 35 EC for 12 days. Methyl parathion did not degrade at 6 EC, while at 

25 EC, methyl aminoparathion, formed from the reduction of the nitro group, was the sole metabolite. At 

35 EC, methyl aminoparathion was formed from the reduction of the nitro group, and 4-nitrophenol was 

formed by hydrolysis. For the 25 EC samples, 50 and 28% of the applied amount remained in the soil by 

day 4 and day 6, respectively. No methyl parathion remained in the soil by day 6 in the 35 EC samples 

(Sharmila et al. 1988). Studies show that methyl parathion forms bound residues in moist soils, and is 

degraded by reduction of the nitro group. The primary metabolites detected were 4-nitrophenol and 

4-aminophenol, which were further transformed to carbon dioxide by the soil microbiota (Ou et al. 1983). 

Biodegradation is affected by temperature, pH, and moisture content of the soil (Adhya et al. 1987; EPA 

1980c; Ou et al. 1983). 
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6. POTENTIAL FOR HUMAN EXPOSURE 

Low concentrations of methyl parathion, such as those associated with normal use, degrade fairly rapidly 

in the environment (EPA 1980c). For example, 75–85% of an applied concentration of 24.5 ppm was 

found to decompose in 52 days (EPA 1980c). Degradation rate is affected by temperature. Studies by 

Baker and Applegate (1970) showed that the methyl parathion loss over a 50-day period increased by a 

factor of 1.3–1.4 when the temperature was increased from 30 to 50 EC. The pH of the soil also affects 

degradation rate, with methyl parathion degrading faster at more alkaline pH values (Adhya et al. 1987). 

When the concentration of methyl parathion is high, as in bulk disposal and spills, degradation appears to 

be significantly retarded (Butler et al. 1981a; EPA 1980c). In a study simulating spill conditions (EPA 

1980c) for an applied concentration of 10,015 ppm methyl parathion, losses of only 0.1% were observed 

after 52 days. In another simulated spill study, 42.7% of a concentration of 48,900 ppm of methyl 

parathion still remained in the soil after 1 year, and 35.8% remained after almost 4 years (Butler et al. 

1981a). 

Direct photolysis does not appear to be a significant transformation process in soils. Only 5–17% of the 

methyl parathion concentration was lost over 50–60 days (half-life equal to 330 days) during a photolysis 

study (Baker and Applegate 1970). 

6.3.2.4 Environmental Media 

Decomposition of methyl parathion was studied in central Greece in apples remaining on trees after 

spraying (emulsifiable concentrate; 40% active ingredient) and in apples harvested and stored under 

ambient-temperature, refrigerated-room temperature, and controlled-atmosphere conditions (Pappas et al. 

1999). Methyl parathion degraded fastest on the apples remaining on the trees. Half-lives were found to 

be 8 days for apples on trees, 45 days for apples stored at ambient conditions, 68 days for apples stored in 

a controlled-atmosphere room, and 62 days for apples stored in a refrigerated room. 

6.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT 

6.4.1 Air 

In a study to determine the concentrations of pesticides in air collected during times of peak pesticide use 

in California, air samples were collected at applications sites and at locations adjacent to the application 

sites (Baker et al. 1996). Of the samples collected adjacent to the application sites, 50% had levels of 

methyl parathion greater than the detectable limit of 0.2 ng/m3

, while 21% had levels of methyl paraoxon 
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6. POTENTIAL FOR HUMAN EXPOSURE 

greater than the detectable limit of 0.2 ng/m3. The maximum amount of methyl parathion detected was 

26 ng/m3

; the maximum amount of methyl paraoxon detected was 4.8 ng/m3. At the application sites, the 

maximum amount of methyl parathion detected was 520 ng/m3

. Air samples collected at the application 

sites were not analyzed for methyl paraoxon. 

Air samples collected in the Sacramento Valley area of California near sites where methyl parathion was 

heavily used on rice were analyzed by Seiber et al. (1989). Methyl parathion concentrations ranged from 

0.2 (minimum detectable level) to 25.67 ng/m3

 depending on the location and time of sampling. Methyl 

paraoxon, the oxygen analog of methyl parathion, was also detected at a maximum of 3.07 ng/m3

. The 

highest concentrations of both compounds were found at sites near locations of heaviest use. 

Airborne pesticide residues were determined from air samples collected along the Mississippi River from 

Louisiana to Minnesota during a 10-day period in June of 1994. Methyl parathion, used throughout 

Mississippi and in parts of Louisiana and Arkansas primarily on cotton, was detected in 8 of the 

10 samples collected over this 10-day study. The maximum concentration (0.30 ng/m3

 detection limit) of 

methyl parathion was 0.85 ng/m3

 (range of 0.05–3.4 ng/m3), and the median concentration was 0.07 ng/m3 

(Majewski et al. 1998). In a similar study conducted in April–September 1995 at urban and agricultural 

sites along the Mississippi River in Mississippi, Iowa, and Minnesota, airborne methyl parathion 

(35 pg/m3

 detection limit) was detected in 70% of the samples collected at the Mississippi agricultural 

site, and was present at the highest level of any of the 19 insecticides monitored in the study, at a 

maximum concentration of 62 ng/m3 (Foreman et al. 2000). In the same study, the median concentration 

of methyl parathion in all agricultural site air samples collected in the study was 2.5 ng/m3

, and methyl 

parathion was detected in the air samples of urban areas at a maximum concentration of 0.99 ng/m3 

(Coupe et al. 2000). 

Atmospheric concentrations of methyl parathion following application of the pesticide to tobacco fields 

were studied by Jackson and Lewis (1978). They found that levels of methyl parathion decreased rapidly 

following application of either the emulsifiable concentrate or the microencapsulated form. Air 

concentrations for the emulsifiable concentrate ranged from 7,408 ng/m3

 immediately following 

application to 13 ng/m3

 9 days later. The corresponding measurements for the microencapsulated form 

were 3,783 and 16 ng/m3

. 
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6. POTENTIAL FOR HUMAN EXPOSURE 

6.4.2 Water 

Several studies have been conducted to measure methyl parathion in streams, rivers, and lakes. A U.S. 

Geological Survey (USGS) of western streams detected methyl parathion in five river samples taken from 

four states during a 14-month period in 1970 and 1971. The amount of methyl parathion detected ranged 

from 0.04 to 0.23 μg/L (Schultz et al. 1973). A later and more extensive USGS study analyzed water 

samples from major rivers of the United States four times yearly in the period of 1975–1985. Of the 

2,861 water samples, 0.1% had detectable levels of methyl parathion (Gilliom et al. 1985). In a study of 

Arkansas surface waters, samples of lake and river/stream water were collected and analyzed over a 

three-year period (Senseman et al. 1997). Of the 485 samples collected, methyl parathion was found in 

one river/stream sample at a maximum concentration of 3.5 μg/L. Results from an EPA study in 

California detected methyl parathion in 3 of 18 surface drain effluent samples at concentrations of 

10–190 ng/kg. Subsurface drain effluent water had concentrations of 10–170 ng/kg in 8 of 60 samples 

(IARC 1983). 

Groundwater has also been surveyed for methyl parathion. In a study of well water in selected California 

communities, methyl parathion was not detected (detection limit of 5 ppb) in the 54 wells sampled 

(Maddy et al. 1982), even though the insecticide had been used in the areas studied for over 15 years. An 

analysis of 358 wells in Wisconsin produced the same negative results (Krill and Sonzogni 1986). In a 

sampling of California well water for pesticide residues, no methyl parathion was detected in any of the 

well water samples (California EPA 1995). In a study to determine the residue levels of pesticides in 

shallow groundwater of the United States, water samples from 1,012 wells and 22 springs were analyzed. 

Methyl parathion was not detected in any of the water samples (Kolpin et al. 1998). In a study of water 

from near-surface aquifers in the Midwest, methyl parathion was not detected in any of the water samples 

from 94 wells that were analyzed for pesticide levels (Kolpin et al. 1995). 

Methyl parathion has been reported in groundwater in Idaho at a median level of 0.01 ppb with 

contamination due to a point source (EPA 1988c). A study of tap water in Ontario showed no detectable 

methyl parathion at a detection limit of 1 ng/L (Le Bel et al. 1979). 

Samples of rainfall in Iowa have been analyzed for levels of pesticides (Nations and Hallberg 1992). 

Samples collected in April, May, and June of the three years in the study period of 1987–1990 had the 

highest levels of methyl parathion, corresponding to the application to crops. Methyl parathion was 

found in 4 of the 318 rain samples analyzed at a maximum concentration of 2.77 μg/L. In a study of 
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6. POTENTIAL FOR HUMAN EXPOSURE 

pesticides in rain and air, conducted in April–September 1995 at urban and agricultural sites along the 

Mississippi River in Mississippi, Iowa, and Minnesota, methyl parathion was present at the highest level 

of any of the 47 pesticides monitored in the rain samples collected in the study (Coupe et al. 2000). 

Methyl parathion was detected in the agricultural and urban site rain samples at maximum concentrations 

of 22.9 μg/L (median of 0.12 μg/L) and 0.3 μg/L (median of 0.024 μg/L), respectively (Coupe et al. 

2000). In the same study, at the agricultural site in Mississippi, the total wet deposition of methyl 

parathion during the 6-month study was 1,740 μg/m2

 (89% of the total wet depositional loading at that 

site), greater than the totals for each of the other 46 compounds monitored in the study (Majewski et al. 

2000). Methyl parathion was not detected in the wet deposition at the Iowa site and was detected only 

once at each of the two Minnesota sites (Majewski et al. 2000). 

Methyl parathion and methyl paraoxon concentrations were measured in the condensate from coastal fog 

in California. Levels ranged from 0.046 to 0.43 μg/L methyl parathion and from 0.039 to 0.49 μg/L 

methyl paraoxon. The authors noted that the transformation of the methyl parathion to the methyl 

paraoxon appeared to take place during atmospheric transport of methyl parathion away from the 

agricultural areas (Schomburg et al. 1991). 

6.4.3 Sediment and Soil 

In random samples of soil taken from five Alabama counties, only 3 of 46 soil samples contained methyl 

parathion. The concentration in these samples was <0.1 ppm (Albright et al. 1974). As part of the 

National Soils Monitoring Program, soil and crop samples from 37 states were analyzed for methyl 

parathion during 1972. Methyl parathion was detected in only 1 soil sample, at a concentration of 

<0.1 ppm and taken from South Dakota, out of 1,246 total samples taken from the 37 states (Carey et al. 

1979). In soil and sediment samples collected from a watershed area in Mississippi, methyl parathion was 

not detected in the soil samples. In three wetland sediment cores, however, measurable concentrations of 

methyl parathion were detected during application season (Cooper 1991). 

A USGS study analyzed bed sediment samples from major rivers of the United States twice yearly in the 

period of 1975–1985. Methyl parathion was not detected in any sediment sample (Gilliom et al. 1985). 

In a study of a highly contaminated soil evaporation pit in California, methyl parathion was found to a 

depth of 90 cm in the soil bed. The concentration at this depth was 18 ppm. Highest concentrations were 

found in the top 7.5 cm of the soil surface and ranged from 32 to 392 ppm (Winterlin et al. 1989). In a 
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6. POTENTIAL FOR HUMAN EXPOSURE 

study to determine if spills caused by poor handling, storage, or containment practices of agricultural 

products released pesticides to soil, samples were collected from agrichemical sites in Illinois (Krapac 

et al. 1995). Of the 822 soil samples collected at 49 sites, methyl parathion was found at 2 of the sites, at 

a median concentration of 112 ppb and a mean concentration of 584 ppb. 

Marine sediments, adjacent to a pesticide manufacturing plant in Denmark, contained methyl parathion 

levels of 40.6 and 44.1 μg/kg dry weight at depths of 0–3 and 4–8 cm, respectively (Kjolholt 1985). 

6.4.4 Other Environmental Media 

Methyl parathion was monitored in crops from 37 states in 1972 as part of the National Soils Monitoring 

Program (Carey et al. 1979). The pesticide was detected in 40% of cotton stalk, 6.3% of cotton seed, 

2.3% of mixed hay, and 9.1% of sorghum samples. Mean concentrations ranged from 0.15 ppm in cotton 

stalks to <0.1 ppm in cotton seeds, mixed hay, and sorghum. The compound has also been reported in the 

outer shuck of sweet corn at a concentration of 0.13–0.14 μg/cm2

, 1–2 days after application, but was not 

detectable in the inner shuck (Wicker et al. 1979). Imported flowers were reported to contain a mean 

concentration of 0.3 mg/kg in 10.5% of samples tested (Morse et al. 1979). 

In a Food and Drug Administration (FDA) summary of the levels of pesticides in ready-to-eat foods in the 

10-year period from 1982 to 1991, methyl parathion was found 12 times in 8 kinds of food, at an average 

concentration of 0.0035 ppm (Kan-Do Office and Pesticides Team 1995). A 5-year analysis of domestic 

and imported foods and animal feeds for the years 1982–1986 detected 94 samples out of 19,851 total 

samples that contained methyl parathion (Hundley et al. 1988). Eighty-nine of the samples had 

concentrations in the range of 0.05–0.5 ppm, and five had levels ranging from 1.0 to 2.0 ppm. Methyl 

parathion was found in celery, citrus, coriander, cantaloupe, Chinese peas, hay, alfalfa feed, Italian 

squash, lettuce, mustard greens, okra, parsley, peppers, spinach, strawberries, tomatillos, and tomatoes. 

An FDA study of pesticide residues in infant and adult foods eaten by infants/children for the period 

1985–1991 reported results for methyl parathion as total parathion (Yess et al. 1993). Of the 2,464 apples 

analyzed, total parathion was detected in 158 samples at a maximum of 1.3 ppm. Of the 862 oranges 

analyzed, total parathion was detected in 25 samples at a maximum of 1.4 ppm. Of the 571 pears 

analyzed, total parathion was detected in 8 samples at a maximum of 0.12 ppm. 

A large study of fruits and vegetables available in Canada examined 5,784 Canadian samples and 

16,198 imported (including from the United States) samples (Neidert and Saschenbrecker 1996). Of the 
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6. POTENTIAL FOR HUMAN EXPOSURE 

Canadian samples analyzed, 1 sample (carrots) contained a methyl parathion residue at a level of 

<0.05 ppm. Of the imported samples, 14 contained methyl parathion residues. Levels of methyl 

parathion ranged from <0.05 ppm (in pears and snowpeas), to 0.10 ppm (in apples, oranges, pears, and 

tomatoes), to a maximum of 0.50 ppm (in grapes, apples, oranges, and pears, plus another unspecified 

sample). 

Citrus fruits from markets in Spain were analyzed for residues of methyl parathion along with other 

organophosphorus insecticides (Torres et al. 1997). Of the 171 orange samples analyzed, 14 had levels of 

methyl parathion <0.2 ppm, while 5 had levels >0.2 ppm. Levels ranged from the 0.1 ppm limit of 

detection to 3.8 ppm depending on the type of orange. Of the 15 grapefruit samples analyzed, 1 was 

found to contain methyl parathion at a level of 0.3 ppm. 

A study of estuarine fish in 21 coastal states conducted from 1972 to 1976 as part of the National 

Pesticide Monitoring Program detected a mean concentration of 47 ppb in 3.9% of the fish tissue samples 

collected (Butler and Schutzmann 1978). In another study (Cooper 1991), fish collected in a watershed 

area of Mississippi were analyzed for residues of methyl parathion. Methyl parathion was detected in 

seven species of fish, with white bass having the greatest mean concentration, at 15.96 ppm. Methyl 

parathion was found in 3 of the 32 fish samples collected before spraying of methyl parathion and in 

12 of the 25 samples of fish collected after methyl parathion spraying. 

Methyl parathion was not detected (detection limit of 1.0 ppb) in a study of 21 market samples and 

4 producer samples of milk obtained in Portugal. However, the oxygen analog and metabolite of methyl 

parathion, methyl paraoxon, was found (detection limit of 1.0 ppb) in 22 of the 25 samples, at 

concentrations ranging from 1.5 to 8.7 ppb, with an average level of 3.6 ppb (Lino and da Silveira 1992). 

All of the market samples contained methyl paraoxon, while only one of the producer samples contained 

the compound. In a study of milk and cheese products obtained in Greece, of the 38 bovine milk samples 

analyzed, two contained methyl parathion at levels that ranged from 43 to 280 ppb of milk fat, with a 

mean concentration of 161 ppb of milk fat (Mallatou et al. 1997). In a study of milk and yogurt samples 

from Egypt, methyl parathion and its metabolites methyl paraoxon and 4-nitrophenol were not detected in 

any of the samples (Ahmed 2000). 

One FDA study (Roy et al. 1997) determined the levels of pesticide residues in rice and apples. Of the 

769 domestic apples analyzed, methyl parathion was found in 72 samples at a maximum concentration of 

0.15 ppm. Of the 1,062 imported apples analyzed, methyl parathion was found in 4 samples at a 
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6. POTENTIAL FOR HUMAN EXPOSURE 

maximum concentration of 0.05 ppm. Of the 598 samples of domestic rice, methyl parathion was found 

in 4 samples at a maximum concentration of 0.13 ppm. Of the 612 imported rice samples analyzed, 

1 sample contained methyl parathion, at a concentration of 0.04 ppm. 

6.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE 

There are insufficient data to determine potential daily inhalation and dermal exposure levels. However, 

based on the information presented in Sections 6.3 and 6.4, exposure levels for the general population are 

probably very low by these routes. Inhalation exposure is not important for the general population, with 

the possible exception of those individuals living near areas where methyl parathion is frequently sprayed. 

Since methyl parathion is readily adsorbed through the skin, dermal contact may be the most relevant 

exposure pathway. Dermal contact is most likely to occur in people who are occupationally exposed. 

In a study to determine if the general population living near an area of heavy pesticide use is exposed to 

high levels of pesticides from foods, the diets of occupants residing in nine homes in the Lower Rio 

Grande Valley were analyzed for residue levels of pesticides (Berry et al. 1997). Food samples obtained 

from markets in Texas or Mexico were analyzed in the summer and spring of the study year. In the 

30 types of food analyzed in the spring and the 24 types analyzed in the summer, methyl parathion was 

detected in 1 food sample at a concentration of 0.018 ppm in the spring and 0.004 ppm in the summer. In 

another study in the Lower Rio Grande Valley region to determine pesticide exposure in certain homes, 

samples of air from both inside and outside the homes and household dust were analyzed (Mukerjee et al. 

1997). Indoor air samples collected in the spring contained methyl parathion at <0.4 ng/m3

, while the 

outdoor air samples contained 0.4 ng/m3

. In the summer, the indoor air samples contained 13.8 ng/m3 

methyl parathion while the outdoor air samples contained 12.4 ng/m3. The household dust was found to 

contain 21 ppb of methyl parathion in both the spring and summer. It is not known at this time if these 

levels are significant. Studies are currently underway to address this issue (EPA 1999b). 

The FDA Total Diet Studies/Market Basket Surveys examine foods for levels of pesticides. Estimates are 

then made of the mean intake of a pesticide (in μg/kg/day) using the amounts of pesticides found in foods 

and food consumption patterns. For the period of 1984–1986, the estimates were <0.0001 μg/kg/day for 

all eight age groups: 6–11 months, 2 years, 14–16 years female, 14–16 years male, 25–30 years female, 

25–30 years male, 60–65 years female, and 60–65 years male (Gunderson 1995a). For the period of 

1986–1991, the estimates were 0.0002 μg/kg/day for the 6–11 months group, 0.0001 μg/kg/day for the 

2 years group, <0.0001 μg/kg/day for the 14–16 years and 25–30 years groups, and 0.0001 μg/kg/day for 
METHYL PARATHION 143 

6. POTENTIAL FOR HUMAN EXPOSURE 

the 60–65 years group (Gunderson 1995b). FDA Market Basket Surveys from 1979 to 1980 and from 

1980 to 1982 estimated mean adult average daily exposure to pesticide residues to be 

0.0126–0.0596 μg/day (Gartrell et al. 1985, 1986). No data indicate that inhalation or dermal exposure 

are concerns for the general population, except for people living near the areas where methyl parathion is 

used. 

Exposure of the general population to higher concentrations of methyl parathion may result from contact 

with, or ingestion of, contaminated hazardous waste site media, principally soils and water. No 

information was found in the available literature regarding the size of the human population potentially 

exposed to methyl parathion through contact with contaminated waste site media. 

NIOSH estimated that approximately 150,000 U.S. workers are potentially exposed to methyl parathion 

in occupational settings (NIOSH 1976). The OSHA workplace air environmental limit of 1.2 mg/m3

 is 

only exceeded for a short while after spraying and only within a short radius of the application area 

(Draper and Street 1981). Exposure is mainly through the dermal route, although inhalation can also be a 

route of exposure. Workers most likely to be exposed are those directly involved with the manufacture, 

application, and cleanup of the chemical, and field workers (NIOSH 1976). Studies on exposure to 

methyl parathion following reentry of workers into a sprayed field showed exposures to be above safe 

levels for up to 48 hours after application (Ware et al. 1973, 1974). Analyses of methyl parathion 

residues on protective garments before and after washing indicate that laundry workers cleaning these 

garments may also be exposed (Hild et al. 1989; Laughlin and Gold 1987, 1989a, 1989b; Leonas et al. 

1989). 

Samples of the indoor and outdoor air at the homes of workers occupationally exposed to pesticides, 

farmers and pesticide formulators, were taken monthly and analyzed for methyl parathion. Methyl 

parathion was found in 13 of 52 indoor air samples of formulators' homes at a mean concentration of 

0.26 μg/m3

 (range of 0.04–9.4 μg/m3). Outdoor air samples of formulators’ homes showed that 3 of 

53 samples contained methyl parathion at concentrations ranging from 0.15 to 0.71 μg/m3

. Methyl 

parathion was not detected in the indoor and outdoor air samples from farmers' homes (Tessari and 

Spencer 1971). 
 

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6. POTENTIAL FOR HUMAN EXPOSURE 

6.6 EXPOSURES OF CHILDREN 

This section focuses on exposures from conception to maturity at 18 years in humans. Differences from 

adults in susceptibility to hazardous substances are discussed in 3.7 Children’s Susceptibility. 

Children are not small adults. A child’s exposure may differ from an adult’s exposure in many ways. 

Children drink more fluids, eat more food, breathe more air per kilogram of body weight, and have a 

larger skin surface in proportion to their body volume. A child’s diet often differs from that of adults. 

The developing human’s source of nutrition changes with age: from placental nourishment to breast milk 

or formula to the diet of older children who eat more of certain types of foods than adults. A child’s 

behavior and lifestyle also influence exposure. Children crawl on the floor, put things in their mouths, 

sometimes eat inappropriate things (such as dirt or paint chips), and spend more time outdoors. Children 

also are closer to the ground, and they do not use the judgment of adults to avoid hazards (NRC 1993). 

Children and the general population living in areas far from where methyl parathion is sprayed are not 

likely to be exposed to high levels of methyl parathion. For those living near the areas where methyl 

parathion is used, the children within the general population are likely to be exposed to methyl parathion 

in the same way as the adults, by contact with sprayed plants, breathing contaminated air, eating 

contaminated foods, or drinking contaminated water. Children living in agricultural areas may be 

exposed to higher pesticide levels than other children because of pesticides that may get tracked into the 

homes by household members, by pesticide spray drift, or from playing in the fields near where methyl 

parathion has been sprayed. Dermal exposure is expected to be the most common route of exposure. 

Methyl parathion has been illegally used inside the home to kill insects (ATSDR 1999; EPA 1999b). 

This practice can result in high exposure levels to the occupants, including children. In an analysis of 

samples taken from a home nearly two weeks after the home had been illegally sprayed with a 4% 

solution of methyl parathion, air samples contained 0.041 mg/m3

, and water samples, collected from water 

kept in an open jar, contained 138–275 ppb (0.138–0.275 mg/kg) (Dean et al. 1984). National Alerts 

published by the EPA and ATSDR (ATSDR 1999; EPA 1999b) on the illegal use of methyl parathion in 

the home state that children are particularly vulnerable to methyl parathion, and deaths have been 

reported. (See also Section 2.2.1.1.) A recent study of U.S. inner-city children’s exposure to pesticides 

states that such children are still being exposed to illegally used pesticides, as when methyl parathion was 

illegally used in cities in 1996, with illegal spraying occurring in 1,100 homes in Chicago, Cleveland, and 

on the Gulf Coast (Landrigan et al. 1999). 
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6. POTENTIAL FOR HUMAN EXPOSURE 

Additionally, children of workers who are exposed to methyl parathion through their employment could 

be exposed to high levels of methyl parathion. The workers in the manufacture, formulation, and use of 

methyl parathion may come into contact with methyl parathion on their skin or clothing. Children who 

reside in the homes of these workers could be exposed to methyl parathion by contact with any methyl 

parathion that might be on the workers’ clothing, hair, or skin, or from contact with tools or other 

contaminated items brought home from work. Also, if children of farm workers enter fields shortly after 

methyl parathion has been applied to crops, they may be exposed to high levels of methyl parathion from 

coming into contact with sprayed plants or by breathing the mist containing methyl parathion. 

Small children are more likely than adults to come into contact with pesticide residues that may be 

present in soil outside the home and in dust inside the home. The tendency for young children to ingest 

soil, either intentionally through pica-related behavior or unintentionally through hand to mouth activity, 

may expose children to residues in the soil. Hand to mouth activity indoors may expose the children to 

residues that may be present in carpets or in dust on uncovered floors. Methyl parathion strongly adsorbs 

to soil, but after being adsorbed, it rapidly degrades. If the children are playing in soil in regions where 

methyl parathion is used on crops, then they may be exposed to elevated levels depending on the amount 

of time that has passed since the spraying has occurred. Since methyl parathion degrades rapidly in soil, 

it is anticipated that soil-borne exposure concentrations will decrease with increasing time from any spray 

event. Children who are playing in soil in regions far from where methyl parathion is used would not be 

expected to be exposed to soil-borne methyl parathion. 

Some quantitative estimates of exposure in the infant and child populations have been reported in a 

number of FDA Total Diet Monitoring Studies conducted in the 1980s using the amounts of pesticide 

residues in foods thought to be in the diets of infants or children. Estimates of the mean intake of methyl 

parathion were made for the 6–11 months age group, 2 years age group, and the 14–16 years female and 

14–16 years male age groups. For the period of 1984–1986, the estimates were <0.0001 μg/kg/day for all 

of the age groups (Gunderson 1995a). For the period of 1986–1991, the estimates were 0.0002 μg/kg/day 

for the 6–11 months group, 0.0001 μg/kg/day for the 2 years group, and <0.0001 μg/kg/day for both the 

female and male 14–16 years groups (Gunderson 1995b). 

An extensive study was undertaken to determine if pesticide residues are present in any infant formula 

products (Gelardi and Mountford 1993). Milk- and soy-based formulas were analyzed, as was the water 

used to make the formula. No pesticide residues, including methyl parathion, were detected in any infant 

formula manufactured in the United States. Thus, it does not appear that infants will be exposed to 
METHYL PARATHION 146 

6. POTENTIAL FOR HUMAN EXPOSURE 

methyl parathion residues through consuming formula. As reported previously, methyl parathion was not 

detected in a study of 21 market samples of milk obtained in Portugal (1 ppm detection limit). However, 

the oxygen analog of methyl parathion, methyl paraoxon, was found in all samples, ranging from 1.5 to 

8.7 ppm, with an average level of 3 ppm (Lino and da Silveira 1992). In the analysis of bovine milk in 

Greece for pesticide residues, 2 of the 38 bovine milk samples had concentrations of methyl parathion 

that ranged from 43 to 280 ppb of milk fat (Mallatou et al. 1997). Samples (9 of 19) of cow’s milk 

obtained from the Central Asian Republic of Kazakhstan were found to contain methyl parathion at 

concentrations that ranged from 3 to 20 ppb (Lederman 1996). These data suggest that milk from animals 

in the United States may also contain low levels of methyl parathion or methyl paraoxon and, thus, that 

children, who typically consume large volumes of milk relative to the general population, may be exposed 

to methyl parathion through milk consumption. 

A potential source of exposure in infants is the presence of methyl parathion in breast milk. No data were 

found in the available literature on the presence of malathion or its residues in breast milk in the United 

States. However, data from foreign countries indicate that methyl parathion residues may be excreted in 

breast milk. In a study of breast milk samples obtained in 1988–1990 from 10 regions within the Central 

Asian Republics of Turkmenistan, Tajikistan, and Kazakhstan, samples from 5 of the regions contained 

methyl parathion residues (Lederman 1996). Of the 90 samples for which data were reported, 8 contained 

methyl parathion, at a range of 1–100 ppb. Methyl parathion was also detected in 11 of 50 breast milk 

samples obtained from two regions in Kazakhstan in 1987 and 1992, at a range of 1.6–80 ppb (Lederman 

1996). In a study of the breast milk of 11 Italian women from which samples were obtained at both the 

5th and 30th day of lactation, methyl parathion was not detected in any of the samples (Roggi et al. 1991). 

6.7 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES 

Those populations most at risk for exposure to high levels of methyl parathion are workers who mix and 

apply the chemical and field workers who go into sprayed areas. Individuals living near the NPL sites 

currently known to be contaminated with methyl parathion and those living near production facilities or 

other point sources might also be at risk for higher exposure. People living in areas very close to 

application sites may be exposed to amounts higher than the general population. In addition, laundry 

workers who wash the garments worn by field workers or by workers involved with mixing and applying 

methyl parathion may be exposed to higher concentrations (Hild et al. 1989; Laughlin and Gold 1987, 

1989a, 1989b; Leonas et al. 1989). 
METHYL PARATHION 147 

6. POTENTIAL FOR HUMAN EXPOSURE 

In a study of 135 workers in the chemical industry who handle methyl parathion, the methyl parathion 

concentration in plasma, the 4-nitrophenol concentration in urine, and the cholinesterase and 

acetylcholinesterase activities were determined to assess the pesticide burden in such workers (Leng and 

Lewalter 1999). The mean concentration of methyl parathion in the plasma of the workers was 233 μg/L; 

no clinical symptoms were reported by the workers. In an additional group of 19 workers handling 

methyl parathion, who were also exposed to the pyrethroid cyfluthrin, the mean concentrations of methyl 

parathion in plasma were 269 and 241 μg/L (for groups without and with clinical symptoms, 

respectively), and 7 of the workers exhibited skin paraesthesia, while none of the 427 workers exposed 

only to the pyrethroid experienced the symptom (Leng and Lewalter 1999). 

Methyl parathion is only for use on agricultural crops. The reports that methyl parathion has been 

illegally/improperly used inside homes to kill insects (ATSDR 1999; EPA 1999b) show that people in 

homes that are sprayed with methyl parathion may be exposed to dangerously high levels of methyl 

parathion. 

The sizes of these populations and the concentrations of methyl parathion in all of the contaminated 

media to which these people would potentially be exposed have not been adequately characterized. 

6.8 ADEQUACY OF THE DATABASE 

Section 104(i)(5) of CERCLA, as amended, directs the Administrator of ATSDR (in consultation with the 

Administrator of EPA and agencies and programs of the Public Health Service) to assess whether 

adequate information on the health effects of methyl parathion is available. Where adequate information 

is not available, ATSDR, in conjunction with the National Toxicology Program (NTP), is required to 

assure the initiation of a program of research designed to determine the health effects (and techniques for 

developing methods to determine such health effects) of methyl parathion. 

The following categories of possible data needs have been identified by a joint team of scientists from 

ATSDR, NTP, and EPA. They are defined as substance-specific informational needs that if met would 

reduce the uncertainties of human health assessment. This definition should not be interpreted to mean 

that all data needs discussed in this section must be filled. In the future, the identified data needs will be 

evaluated and prioritized, and a substance-specific research agenda will be proposed. 
 

 

METHYL PARATHION 148 

6. POTENTIAL FOR HUMAN EXPOSURE 

6.8.1 Identification of Data Needs 

Physical and Chemical Properties. The physical and chemical properties of methyl parathion are 

sufficiently well characterized to allow assessment of the environmental fate of the compound to be made 

(Budavari 1989; EPA 1980c; Hawley 1987; Keith and Walters 1985; NFPA 1986; Ruth 1986; Sanders 

and Seiber 1983; Schimmel et al. 1983; Sunshine 1969; Tomlin 1994; Weiss 1986). 

Production, Import/Export, Use, Release, and Disposal. Methyl parathion is commercially 

produced in the United States and abroad. Since 1977, production volume statistics for methyl parathion 

have been combined with those of ethyl parathion, also known as parathion. In 1983, the combined 

production capacity was estimated at 29 million kg for the United States and 10–15 million kg for western 

Europe (IARC 1983). Data on recent production in the United States were not located. In 1980, 

413,000 kg of methyl parathion were imported (USITC 1981). Exports in 1984 amounted to 

5.68 million kg (Bureau of the Census 1984). More current information on the manufacture, import, and 

export of the insecticide are needed so that an assessment can be made of potential human exposure to 

methyl parathion. 

The use of methyl parathion as a broad-spectrum insecticide for a variety of food and nonfood crops, 

ornamentals, trees, and mosquito breeding areas is well documented (IARC 1983; International Labour 

Office 1983; Meister 1988; NPIRS 1986; Spencer 1982; Tomlin 1994; Weir and Hazleton 1981). While 

the annual use of methyl parathion, a restricted-use compound, in the United States has also been well 

documented in general (EPA 1999c; Giannessi and Anderson 1995), there are few studies that document 

the illegal use of the compound in the home (Landrigan et al. 1999). It would be helpful to have an 

estimate of the amounts of methyl parathion used illegally in the home and the frequency of these usages 

so that the potential for exposure to children in such homes can be assessed. It would also be helpful to 

have updated use information that was collected after EPA cancelled many of the food crop uses of the 

compound, including on several crops commonly eaten by children (EPA 1999d; 1999e). 

Releases to air, land, and water occur primarily through its use as a restricted-use insecticide. The media 

of most importance for human exposure are contaminated air and soil. According to the Emergency 

Planning and Community Right-to-Know Act of 1986, 42 U.S.C. Section 11023, industries are required 

to submit chemical release and off-site transfer information to the EPA. The Toxic Release Inventory 

(TRI), which contains this information for 1987, became available in May of 1988. This database is 

updated yearly and provides a list of industrial production facilities and emissions. 
 

 

 

METHYL PARATHION 149 

6. POTENTIAL FOR HUMAN EXPOSURE 

Methods suggested for the disposal of methyl parathion are incineration and open field burial at 

designated landfills (EPA 1974a). In the past, improved methods for the disposal of methyl parathion 

were being considered (EPA 1981b). Regulations pertaining to the disposal of methyl parathion include 

the requirement that containers contaminated with methyl parathion residues be emptied, decontaminated, 

and either recycled, incinerated, or disposed of in a landfill depending on their condition (EPA 1974a). 

No recent data are available. Thus, further information on the optimal method for disposal of methyl 

parathion is needed to evaluate the potential for the release of and exposure to methyl parathion. 

Environmental Fate. While methyl parathion degrades fairly rapidly and is relatively immobile in 

the environment at lower concentrations, there is still some uncertainty regarding the degradation and 

mobility of very high concentrations of methyl parathion, such as might be found at spill sites, and at 

pesticide disposal and other hazardous waste sites (Albanis et al. 1988b; Butler et al. 1981a; EPA 1980c; 

Jury et al. 1987a; Rao and Davidson 1979). Further studies with high concentrations of methyl parathion 

are needed to assess the environmental fate of the compound in these particular situations. Additional 

studies of methyl parathion degradation in air, particularly to methyl paraoxon, and the subsequent 

degradation of methyl paraoxon, are needed to better assess releases to air. Additionally, the methyl 

aminoparathion metabolite, which forms under anaerobic soil conditions, binds strongly to organic matter 

(Sharmila et al. 1988). Studies on the fate of methyl aminoparathion and the potential for it to become 

oxidized to methyl parathion are needed to characterize the fate of methyl parathion in the environment. 

Bioavailability from Environmental Media. Methyl parathion can be absorbed following 

inhalation or dermal contact with contaminated air and by ingestion of contaminated water or food (Dean 

et al. 1984; Fazekas 1971; Morgan et al. 1977; Nemec et al. 1968; Ware et al. 1973, 1974, 1975). Dermal 

contact with or ingestion of methyl parathion that is tightly bound to soil particles is an exposure route of 

concern at hazardous waste sites and areas where spills have occurred. No information is available on the 

absorption of methyl parathion from soil following ingestion or dermal contact with contaminated soils. 

Therefore, additional information is needed on the uptake of methyl parathion from contaminated soil 

following ingestion or dermal contact. 

Food Chain Bioaccumulation. There are a few studies to determine residues of methyl parathion in 

organisms in the environment. These have consistently shown low methyl parathion residues, indicating 

that methyl parathion does not bioconcentrate to a significant extent in aquatic organisms, plants, or 

animals (Crossland and Bennett 1984; Sabharwal and Belsare 1986). The methyl parathion that does get 

into organisms is rapidly degraded (Sabharwal and Belsare 1986). Some recent analyses of fish in a 
 

 

METHYL PARATHION 150 

6. POTENTIAL FOR HUMAN EXPOSURE 

watershed region in the United States indicates ppm (16 μg/g) levels of methyl parathion suggesting that 

methyl parathion sometimes persists long enough for uptake by fish to occur, and thus, could possibly 

play a role in bioaccumulation (Cooper 1991). Additional studies to verify that bioaccumulation is not 

occurring are needed. 

Exposure Levels in Environmental Media. Methyl parathion has been detected in ambient air 

(Baker et al. 1996; Jackson and Lewis 1978; Majewski et al. 1998; Seiber et al. 1989), surface water 

(Gilliom et al. 1985; Senseman et al. 1997), groundwater (EPA 1988c), rainfall (Nations and Halbert 

1992), coastal fog (Schomburg et al. 1991), soil (Albright et al. 1974; Carey et al. 1979; Krapac et al. 

1995; Winterlin et al. 1989), sediments (Cooper 1991), fish (Butler and Schutzmann 1978; Cooper 1991), 

and foodstuffs (Neidert and Saschenbrecker 1996; Torres et al. 1997). Estimates of human intake of 

methyl parathion have been made for ingestion of foodstuffs (Gartrell et al. 1985, 1986), but improved 

estimates of exposure from air, water, and soil are needed to assess human exposure to methyl parathion. 

Information concerning concentrations in the air, water, and soil at the NPL hazardous waste sites known 

to be contaminated with these compounds are needed to estimate the exposure of populations living in the 

vicinity of these sites. 

Exposure Levels in Humans. Methyl parathion has been detected in serum and tissue shortly after 

acute exposure (EPA 1978e; Ware et al. 1975). It is rapidly metabolized and does not persist in serum 

and tissues for long (Braeckman et al. 1983). Two metabolites of methyl parathion, 4-nitrophenol and 

dimethyl phosphate, can be detected in urine and tissues for up to 2 days following exposure (Morgan et 

al. 1977). These compounds are specific for methyl parathion when there is a history of exposure. 

Methyl parathion has been detected in blood within 1 day of exposure and is a specific biomarker 

(Fazekas 1971). 

A recent method to screen the urine for alkyl phosphates as an indicator of exposure to organophosphate 

insecticides shows that the method can be used to determine environmental exposure to a specific 

organophosphate pesticide. The method was found to be sensitive, identifying low levels of exposure to 

insecticides in the environment by quantitation of urinary phosphates (Davies and Peterson 1997). The 

test is limited in that it is only useful for assessing recent exposure, due to the short half-life of the 

organophosphate pesticides. 

A recent method, still in development, for determining total 4-nitrophenol in the urine of persons exposed 

to methyl parathion is based on solid phase microextraction (SPME) and GC/MS; previously, the method 
 

 

METHYL PARATHION 151 

6. POTENTIAL FOR HUMAN EXPOSURE 

has been used in the analysis of food and environmental samples (Guidotti et al. 1999). The method 

shows promise for use in determining exposures at low doses, as it is very sensitive. There is a need for 

additional development of this method, as the measurement of acetylcholinesterase (the enzyme inhibited 

by exposure to organophosphates such as methyl parathion) is not an effective indicator of low-dose 

exposures. 

Exposures of Children. More studies are needed to assess the exposures of children living in 

agricultural areas to methyl parathion residues in air, soil, or water. More studies are also needed to 

assess the exposures of children in the general population to residues of methyl parathion that might be 

present in food, milk, or water, or on contaminated clothing and skin from occupationally exposed 

household members. 

Additional studies to determine breast milk contamination by methyl parathion are needed to be able to 

assess exposures to nursing infants. 

Child health data needs relating to susceptibility are discussed in 3.12.2 Identification of Data Needs: 

Children’s Susceptibility. 

Exposure Registries. No exposure registries for methyl parathion were located. This substance is 

not currently one of the compounds for which a subregistry has been established in the National Exposure 

Registry. The substance will be considered in the future when chemical selection is made for 

subregistries to be established. The information that is amassed in the National Exposure Registry 

facilitates the epidemiological research needed to assess adverse health outcomes that may be related to 

exposure to methyl parathion. 

6.8.2 Ongoing Studies 

The Federal Research in Progress (FEDRIP) database provides additional information from a few 

ongoing studies that may fill in some of the data needs identified in Section 6.8.1. These studies are 

summarized in Table 6-2. 

No ongoing studies regarding release, disposal, environmental fate, bioavailability, bioaccumulation, 

exposure levels, or exposure registries were located. 
METHYL PARATHION 152 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-2. Ongoing Studies of Methyl Parathion Found in 

Federal Research in Progress
 

Investigator Affiliation Research description 

Brindley, WA USDA	 Planning insecticide resistance management for methyl parathion. 

Chambers, HW USDA	 Investigation of the nature of esterases involved in 

organophosphate detoxification including methyl parathion. 

Johnson, SJ USDA	 To determine the resistance by soybean looper insects to methyl 

parathion and permethrin. 

Meinke, LJ USDA	 To study the influence of methyl parathion on western corn 

rootworm behavior and population dynamics. 

Meinke, LJ USDA	 Western corn rootworm resistance to methyl parathion– 

development of resistance management strategies 

Nesheim, ON USDA	 To collect, develop, and maintain information related to pesticides 

and the crops on which they are used for the state of Florida. 

Obendorf, SK USDA	 Methods to limit worker exposure to various pesticides, including 

methyl parathion. 

Webster, E USDA	 To collect, develop, and maintain information related to pesticides 

and the crops on which they are used for the state of Arkansas. 

Wild, JR USDA	 To develop an effective and complete biological remediation 

system capable of hydrolyzing organophosphorous neurotoxins 

from agricultural and chemical warfare munitions, contaminations, 

and wastes.

 Wright, RJ USDA	 To document the extent of adult corn rootworm beetles resistence 

to methyl parathion throughout Nebraska. 

USDA = United States Department of Agriculture 
METHYL PARATHION 153 

6. POTENTIAL FOR HUMAN EXPOSURE 

Ongoing remedial investigations and feasibility studies conducted at the NPL sites known to be 

contaminated with methyl parathion will add to the available database on exposure levels in 

environmental media, exposure levels in humans, and exposure registries. 

METHYL PARATHION 155 

7. ANALYTICAL METHODS 

The purpose of this chapter is to describe the analytical methods that are available for detecting, 

measuring, and/or monitoring methyl parathion, its metabolites, and other biomarkers of exposure and 

effect to methyl parathion. The intent is not to provide an exhaustive list of analytical methods. Rather, 

the intention is to identify well-established methods that are used as the standard methods of analysis. 

Many of the analytical methods used for environmental samples are the methods approved by federal 

agencies and organizations such as EPA and the National Institute for Occupational Safety and Health 

(NIOSH). Other methods presented in this chapter are those that are approved by groups such as the 

Association of Official Analytical Chemists (AOAC) and the American Public Health Association 

(APHA). Additionally, analytical methods are included that modify previously used methods to obtain 

lower detection limits and/or to improve accuracy and precision. 

7.1 BIOLOGICAL SAMPLES 

The primary method for detecting methyl parathion and metabolites in biological tissues is gas 

chromatography (GC) coupled with electron capture (ECD), flame photometric (FPD), or flame 

ionization detection (FID). Sample preparation for methyl parathion analysis routinely involves 

extraction with an organic solvent (e.g., acetone or benzene), centrifugation, concentration, and 

resuspension in a suitable solvent prior to GC analysis. For low concentrations of methyl parathion, 

further cleanup procedures, such as column chromatography on silica gel or Florisil are required. 

Table 7-1 summarizes the analytical methods used to detect methyl parathion and its metabolites in 

biological tissues and fluids. 

Methyl parathion was determined in dog and human serum using a benzene extraction procedure followed 

by GC/FID detection (Braeckman et al. 1980, 1983; DePotter et al. 1978). An alkali flame FID (nitrogenphosphorus) detector increased the specificity of FID for the organophosphorus pesticides. The detection 

limit was in the low ppb (μg/L). In a comparison of rat blood and brain tissue samples analyzed by both 

GC/FPD and GC/FID, Gabica et al. (1971) found that GC/FPD provided better specificity. The minimum 

detectable level for both techniques was 3.0 ppb, but GC/FPD was more selective. The EPArecommended method for analysis of low levels (<0.1 ppm) of methyl parathion in tissue, blood, and 

urine is GC/FPD for phosphorus (EPA 1980d). Methyl parathion is not thermally stable above 120 °C 

(Keith and Walters 1985). 
Table 7-1. Analytical Methods for Determining Methyl Parathion and Metabolites in Biolog

Sample matrix Preparation method 

Analytical method 

Sample detection limit 

Percent recovery Refer

Urine Acidify and heat to hydroloyze; add NaOH 

to pH=11; extract with benzene-diethyl ether; reacidify and dry with sodium sulfate; derivatize with hexamethyl disilizane on GC column (PNP) 

GC/ECD 50 μg/L (50 ppb) 95.4 Cranm

EPA 1

Urine Acidify and heat to hydrolyze; add NaOH 

extract with anhydrous ethyl ether; derivatize with diazoethane; concentrate; add hexane; concentrate and cleanup on silica gel; elute with benzene-hexane (PNP) 

GC/ECD 20 μg/L (20 ppb) 85–98 Shafik 

Urine, blood, tissues 

Add acetone; centrifuge; extract on ion exchange column; derivatize with diazopentane; cleanup on silica gel if needed (metabolites) 

GC/FPD 40–150 μg/L 

(40–150 ppb) 

36–97 EPA 1

Lores 

Blood, tissues Homogenize, if tissue; mix sample with 

acetone; centrifuge; concentrate; saturate with sodium chloride; evaporate organic layer; cleanup on silica gel eluting with hexane-benzene; concentrate 

GC/FPD <100 ppb No data EPA 1

Serum Extract with benzene; dry; resuspend in 

ethyl acetate 

GC/FID 2 μg/L (2 ppb) 57–109 Braec

DePo

EDC = electron capture detector; FID = flame ionization detector; FPD = flame photometric detector; GC = gas chromatography; NaOH PNP = paranitrophenol 
METHYL PARATHION 157 

7. ANALYTICAL METHODS 

Methyl parathion rapidly forms hydrolysis products after absorption by the body. 4-Nitrophenol and the 

alkyl phosphate, dimethyl phosphate, are major metabolites that are frequently found in biological fluids 

and tissues following exposure. Sample preparation steps are generally more extensive for the 

metabolites than for the parent compound. Usually, several extractions and a derivation are required prior 

to GC analysis. Total 4-nitrophenol has been measured in human and rat urine using GC/ECD of the 

diazoethane or hexamethyl disilizane derivatives of 4-nitrophenol (Cranmer 1970; Morgan et al. 1977; 

Shafik et al. 1973b). The minimum detectable level was 0.02 ppm. For the analysis of 4-nitrophenol in 

biological tissues and fluids, EPA recommends extraction with benzene-ether and derivatization with 

hexamethyl disilizane prior to analysis by GC/ECD (EPA 1980d). The diazoethane derivative of 

dimethyl phosphate was quantitatively measured in human urine by GC/FPD in the phosphorus mode 

(Morgan et al. 1977). EPA recommends GC/FPD for the detection of the diazopentane derivatives of 

dimethyl phosphate and other alkyl phosphates. Diazopentane derivatives are more easily resolved and 

separated from interfering compounds than diazoethane derivatives. The detection limit of dimethyl 

phosphate by the EPA method was 0.04–0.15 ppm (EPA 1980d; Lores and Bradway 1977; Shafik et al. 

1973a). The problem with the use of the above metabolites for the analysis of methyl parathion exposure 

is that they are not specific. Other organophosphate insecticides may also form these degradates. 

A recent method, still in development, for determining total 4-nitrophenol in the urine of persons exposed 

to methyl parathion is based on solid phase microextraction (SPME) and GC/MS; previously, the method 

has been used in the analysis of food and environmental samples (Guidotti et al. 1999). The method uses 

a solid phase microextraction fiber, is inserted into the urine sample that has been hydrolyzed with HCl at 

50 EC prior to mixing with distilled water and NaCl and then stirred (1,000 rpm). The fiber is left in the 

liquid for 30 minutes until a partitioning equilibrium is achieved, and then placed into the GC injector 

port to desorb. The method shows promise for use in determining exposures at low doses, as it is very 

sensitive. There is a need for additional development of this method, as the measurement of acetylcholinesterase, the enzyme inhibited by exposure to organophosphates such as methyl parathion, is not an 

effective indicator of low-dose exposures. 

Organophosphates, such as methyl parathion, are known to inhibit cholinesterase activity. A method has 

been developed to measure the extent of this inhibition and relate it to organophosphate exposure (EPA 

1980d; Nabb and Whitfield 1967). In this EPA-recommended method, blood is separated into plasma and 

red blood cell fractions. The fractions are treated with saline solution, brought to pH 8 with sodium 

hydroxide, and dosed with acetylcholine perchlorate. The ensuing acetic acid releasing enzyme reaction 
METHYL PARATHION 158 

7. ANALYTICAL METHODS 

is automatically titrated using an automatic titrator. This method is sensitive, simple, and fast, but is not 

specific for methyl parathion. 

In a study of the metabolism of methyl parathion in intact and subcellular fractions of isolated rat 

hepatocytes, a high performance liquid chromatography (HPLC) method has been developed that 

separates and quantitates methyl parathion and six of its hepatic biotransformation products (Anderson et 

al. 1992). The six biotransformation products identified are methyl paraoxon, desmethyl parathion, 

desmethyl paraoxon, 4-nitrophenol, p-nitrophenyl glucuronide, and p-nitrophenyl sulfate. This method is 

not an EPA or other standardized method, and thus it has not been included in Table 7-1. 

7.2 ENVIRONMENTAL SAMPLES 

The predominant method of analyzing environmental samples for methyl parathion is by GC. The 

detection methods most used are FID, FPD, ECD, and mass spectroscopy (MS). HPLC coupled with 

ultraviolet spectroscopy (UV) or MS has also been used successfully. Sample extraction and cleanup 

varies widely depending on the sample matrix and method of detection. Several analytical methods used 

to analyze environmental samples for methyl parathion are summarized in Table 7-2. 

In air, methyl parathion has been determined to the sub-ppt (ng/m3

) level by GC equipped with FPD or a 

nitrogen-phosphorus detector (NPD). Sample preparation methods varied from simple extraction and 

concentration (EPA 1980d, 1987d; Jackson and Lewis 1978; Seiber et al. 1989) to inclusion of column 

cleanup and fractionation steps (Stanley et al. 1971; Tessari and Spencer 1971). The widest variation in 

methods centered around sample collection. Multilevel collectors (EPA 1980d; Jackson and Lewis 1978; 

Stanley et al. 1971), resins (Seiber et al. 1989), and nylon cloth (Tessari and Spencer 1971) have all been 

used successfully. Recoveries ranged from 53 to over 100%. The best recovery and sensitivity data was 

reported by Seiber et al. (1989) during studies of atmospheric methyl parathion concentrations in the 

Sacramento Valley area of California. Using a macroreticular resin sampler, extraction with ethyl acetate, 

and GC/NPD analysis, over 85% of injected methyl parathion was recovered with a sensitivity of 

0.2 ng/m3

 (sub-ppt). However, the precision of the method was low. The EPA-recommended method is 

similar, employing a glass fiber filter/solid sorbent sampler, extraction with diethyl ether in hexane, and 

analysis by GC/FPD (EPA 1980d). Both of these methods detect methyl paraoxon, the oxidized 

metabolite of methyl parathion, as well. Methyl parathion has also been detected in hazardous waste 

incinerator effluents. Using GC/FID and GC/MS, detection limits of 4.8 and 2.0 ng and precisions of 

6 and 10%, respectively, were achieved (James et al. 1985). 
Table 7-2. Analytical Methods for Determining Methyl Parathion in Environmental S

Analytical Sample detection Percent 

Sample matrix Preparation method method limit recovery ReferAir Air Air Water (run-off) Water Water Water, plant tissue Sediments Water, plant tissue, animal tissue 

Collect on hexylene glycol-alumina 

adsorbent sampler; extract; cleanup with Florisil 

Collect on XAD-4 macroreticular 

resin; extract with ethyl acetate 

Collect on solid sorbent; extract with 

diethyl ether in hexane Collect on XAD-2 macroreticular resin; extract with diethyl ether Extract with benzene plus anhydrous potassium carbonate; concentrate; cleanup on silica gel 

Extract with methylene chloride; 

concentrate; cleanup on silica gel Extract with acetonitrile; filter if necessary 

Dry with sodium sulfate; extract with 

acetone/methylene chloride; concentrate Extract with hexane; cleanup with hexane/acetonitrile 

GC/FPD GC/NPD GC/FPD HPLC/UVGC/ECDGC/FPD HPLC/UV/EC GC/FPD GC/ECD

0.1 ng/m3 

0.2 ng/m3 

No data 

2–3 μg/L 

0.1 μg/L 

No data 

No data (water); 

50 μg/kg (plants) 

No data 

0.1 μg/L (water); 0.01 mg/kg (tissue) 

53.4 85–111 

72–105 

99.75 

79 

93 

95–99 73–95 100 

Stanle

Seibe

EPA 1

Pasch

Lee e

EPA 1

Clark 

Belisl

Kadou
Table 7-2. Analytical Methods for Determining Methyl Parathion in Environmental Sample

Sample matrix Preparation method 

Analytical method 

Sample detection limit 

Percent recovery Refer

Plant tissue Extract with ethyl acetate and 

sodium sulfate; filter through silanized glass wool 

GC/TID No data No data AOAC 

Food (butter fat) Extract and cleanup on 

semipreparative HPLC column; elute with methylene chloride-hexane 

GC/ECD No data No data Gilles

EC = electrical conductivity detector; ECD = electron capture detector; FPD = flame photometric detector; GC = gas chromatography; H

liquid chromatography; NPD = nitrogen phosphorus detector; TID = thermionic detector; UV = ultraviolet spectroscopy 
METHYL PARATHION 161 

7. ANALYTICAL METHODS 

Analysis of water for methyl parathion in the ppb (ng/L) range has been done using GC/ECD, GC/FPD, 

and HPLC/UV. With water samples, the primary problems are concentration of the sample and 

selectivity of the method. Water samples generally contain only trace amounts of methyl parathion. 

Usually, other pesticides and interfering compounds are present. Several concentration, cleanup, and 

separation techniques have been tested in an attempt to improve the sensitivity and selectivity of analysis 

by GC/ECD (Agostiano et al. 1983; Kadoum 1968; Kawahara et al. 1967; Le Bel et al. 1979; Lee et al. 

1984). EPA recommends fractionation on silica gel prior to detection by GC/FPD. The FPD detector is 

selective for organophosphates. Recoveries for these methods ranged from 74 to 94% with detection 

limits in the sub- and low-ppb range. HPLC/UV and HPLC/UV/electrochemical detectors have been 

used to simplify sample preparation and increase selectivity (Clark et al. 1985; Paschal et al. 1977). High 

recoveries (>99%) and precision, as well as detection limits in the low-ppb range, were reported. 

Analysis of methyl parathion in sediments, soils, foods, and plant and animal tissues poses problems with 

extraction from the sample matrix, cleanup of samples, and selective detection. Sediments and soils have 

been analyzed primarily by GC/ECD or GC/FPD. Food, plant, and animal tissues have been analyzed 

primarily by GC/thermionic detector or GC/FPD, the recommended methods of the Association of 

Official Analytical Chemists (AOAC). Various extraction and cleanup methods (AOAC 1984; Belisle 

and Swineford 1988; Capriel et al. 1986; Kadoum 1968) and separation and detection techniques (Alak 

and Vo-Dinh 1987; Betowski and Jones 1988; Clark et al. 1985; Gillespie and Walters 1986; Koen and 

Huber 1970; Stan 1989; Stan and Mrowetz 1983; Udaya and Nanda 1981) have been used in an attempt 

to simplify sample preparation and improve sensitivity, reliability, and selectivity. A detection limit in 

the low-ppb range and recoveries of 100% were achieved in soil and plant and animal tissue by Kadoum 

(1968). GC/ECD analysis following extraction, cleanup, and partitioning with a hexane-acetonitrile 

system was used. 

Using a simple, modified GC method with nitrogen-phosphorus detection (GC/NPD), Pappas et al. (1999) 

determined methyl parathion residues in apples with a recovery of 88–108% and a limit of detection of 

2 ppb. Recent work by Sheridan and Meola (1999) suggests that analysis using GC coupled with tandem 

or ion trap MS (MS/MS) is a highly selective method capable of achieving clear compound identification 

and identity confirmation, with identification of compounds present in agricultural samples at the ppb 

level. The method is not as susceptible to interfering co-extractives as methods involving selective 

detectors; GC/MS/MS was able to detect methyl parathion in pears down to 2 ppb, while a selective 

detection method was limited to the level “<3 ppb” (Sheridan and Meola 1999). 
METHYL PARATHION 162 

7. ANALYTICAL METHODS 

Using established extraction and cleanup methods, followed by GC/FPD and GC/thermionic detection, 

Carey et al. (1979) obtained detection limits in the ppb range and recoveries of 80–110% in soil and 

70–100% in plant tissue. Good sensitivity and recovery were maintained in a simplified extraction 

procedure of sediments followed by GC/FPD analysis (Belisle and Swineford 1988). Bound methyl 

parathion residues that were not extracted with the usual methods were extracted using supercritical 

methanol by Capriel et al. (1986). They were able to remove 38% of the methyl parathion residues bound 

to soil, but 34% remained unextractable, and 28% could not be accounted for. 

HPLC has been recommended as a cleanup and fractionation procedure for food samples prior to analysis 

by GC/ECD (Gillespie and Walters 1986). The advantages over the AOAC-recommended Florisil 

column are that it is faster, requires less solvent, and gives better resolution. HPLC coupled with various 

detectors MS, MS/MS, UV/electrochemical detector, or UV/polarographic detection has been tested as a 

rapid, simplified separation and detection system to replace GC (Betowski and Jones 1988; Clark et al. 

1985; Koen and Huber 1970). Recoveries, detection limits, and precisions were generally good, but 

further work is needed before the techniques are adopted for general use. 

7.3 ADEQUACY OF THE DATABASE 

Section 104(i)(5) of CERCLA, as amended, directs the Administrator of ATSDR (in consultation with the 

Administrator of EPA and agencies and programs of the Public Health Service) to assess whether 

adequate information on the health effects of methyl parathion is available. Where adequate information 

is not available, ATSDR, in conjunction with the NTP, is required to assure the initiation of a program of 

research designed to determine the health effects (and techniques for developing methods to determine 

such health effects) of methyl parathion. 

The following categories of possible data needs have been identified by a joint team of scientists from 

ATSDR, NTP, and EPA. They are defined as substance-specific informational needs that, if met, would 

reduce or eliminate the uncertainties of human health assessment. In the future, the identified data needs 

will be evaluated and prioritized, and a substance-specific research agenda will be proposed. 
 

 

METHYL PARATHION 163 

7. ANALYTICAL METHODS 

7.3.1 Identification of Data Needs 

Methods for Determining Biomarkers of Exposure and Effect. Sensitive, accurate methods 

exist for the measurement of erythrocyte and plasma cholinesterase levels (EPA 1980d; Nabb and 

Whitfield 1967). Organophosphates, including methyl parathion, inhibit cholinesterases. There are some 

problems with the reliability of this method because normal erythrocyte cholinesterase values vary widely 

(Midtling et al. 1985; Tafuri and Roberts 1987) and plasma cholinesterase can be suppressed by a variety 

of diseases (Henry 1984; Tafuri and Roberts 1987). Further studies to improve the reliability of 

cholinesterase levels might be useful in establishing this as a reliable measure of organophosphate 

exposure. Studies are needed regarding the measurement of methyl paraoxon in biological tissues, as this 

is the most toxic metabolite of methyl parathion. 

Sensitive analytical methods exist to measure methyl parathion (Braeckman et al. 1980; DePotter et al. 

1978; EPA 1980d) and some of its metabolic products (Anderson et al. 1992; Cranmer 1970; EPA 1980d; 

Lores and Bradway 1977; Morgan et al. 1977; Shafik et al. 1973b) at background levels and levels at 

which biological effects occur. The most sensitive and selective method for methyl parathion is currently 

GC/FPD (EPA 1980d; Gabica et al. 1971). The most sensitive and selective method for metabolites is 

derivitization followed by GC/FPD analysis (EPA 1980d; Lores and Bradway 1977); however, the 

metabolites found following methyl parathion exposure are not specific for methyl parathion. 

Methods for Determining Parent Compounds and Degradation Products in Environmental 

Media. Analytical methods exist to measure low levels of methyl parathion in air (EPA 1980d, 1987d; 

Jackson and Lewis 1978; Seiber et al. 1989; Stanley et al. 1971; Tessari and Spencer 1971), water 

(Agostiano et al. 1983; Clark et al. 1985; Kadoum 1968; Kawahara et al. 1967; Le Bel et al. 1979; Lee et 

al. 1984), soil, and other media (Alak and Vo-Dinh 1987; AOAC 1984; Belisle and Swineford 1988; 

Betowski and Jones 1988; Capriel et al. 1986; Carey et al. 1979; Clark et al. 1985; Gillespie and Walters 

1986; Kadoum 1968; Koen and Huber 1970; Stan 1989; Stan and Mrowetz 1983; Vdaya and Nanda 

1981). These methods can be used to identify potentially contaminated areas to determine if there is a 

risk to human health. The media of most concern for human exposure are air, water, and soil. Sensitive 

methods exist to measure both background levels and levels at which health effects occur. Gas 

chromatography continues to be the most frequently used technique for the separation and identification 

of methyl parathion. Paired with an ECD or FPD, the detection limit is generally in the low- to sub-ppb 

range for air (EPA 1980d), water (Agostiano et al. 1983; Clark et al. 1985; Kadoum 1968; Kawahara et 

al. 1967; Le Bel et al. 1979; Lee et al. 1984), soil, and plant and animal tissue (Belisle and Swineford 
METHYL PARATHION 164 

7. ANALYTICAL METHODS 

1988; Carey et al. 1979; Kadoum 1968). Some problems still exist with sample preparation and 

separation, which affect the precision, accuracy, and specificity of analyses. Further studies to improve 

sample preparation and selectivity of detection might be beneficial in improving the reliability of existing 

methods. 

7.3.2 Ongoing Studies 

No ongoing studies concerning the methods of analysis of methyl parathion in biological samples and 

environmental media were located. 
METHYL PARATHION 165 

8. REGULATIONS AND ADVISORIES
 

The international, national, and state regulations and guidelines regarding methyl parathion in air, water, 

and other media are summarized in Table 8-1. 

Methyl parathion is a restricted-use pesticide (EPA 1985b, 1999a). Methyl parathion formulations must 

be used under the direct supervision of a certified pesticide applicator (EPA 1980b). The certified 

pesticide applicator must be physically present during mixing, loading, application, equipment repair, and 

equipment cleaning (NPIRS 1986). Originally, no worker was allowed to enter a field treated with 

methyl parathion less than 48 hours after the treatment (EPA 1980b); that interval has been increased to 

4–5 days (EPA 1999d). Methyl parathion is not registered for use by homeowners or for use indoors. 

EPA (1999d, 1999e) has canceled many food crop uses of methyl parathion, including uses on fruits and 

vegetables commonly eaten by children (apples, peaches, pears, grapes, nectarines, cherries, plums, 

carrots, succulent peas and beans, and tomatoes) and some other vegetables, and some nonfood uses such 

as ornamental plants and nursery stock uses. Pesticide tolerances on these food crops also have been 

canceled for methyl parathion (EPA 2001). The cancellations occurred because of a concern for risks to 

children and workers. Existing stocks of methyl parathion products with canceled crop uses were allowed 

to be applied through December 31, 1999 (EPA 1999d). As listed in Table 8-1, tolerances have been 

retained for a large number of raw agricultural commodities (EPA 2001). 

ATSDR has derived an intermediate-duration oral MRL of .0007 mg/kg/day for methyl parathion based 

on a minimal LOAEL of 0.22 mg/kg/day for electrophysiological effects in the central and peripheral 

nervous systems in rats (Desi et al. 1998). 

ATSDR has derived a chronic-duration oral MRL of .0003 mg/kg/day for methyl parathion based on a 

NOAEL of 0.025 mg/kg/day for reduced hematocrit and erythrocyte counts in rats (Suba 1984). 

EPA has derived an RfD of .00025 mg/kg/day, based on a NOAEL of 0.025 for reduced hematocrit, 

erythrocyte counts, and hemoglobin (cholinesterase inhibition was also listed as a critical effect but the 

reason for this was not explained). This NOAEL appears to be from the same study as for the ATSDR 

chronic-duration oral MRL, although the study is referenced differently (IRIS 2001). 
METHYL PARATHION 166 

8. REGULATIONS AND ADVISORIES 

Table 8-1. Regulations and Guidelines Applicable to Methyl Parathion 

Agency Description	 Information References 

INTERNATIONAL 

Guidelines: 

IARC Carcinogenic classification Group 3a IARC 2001 

WHO No evidence of carcinogenicity	 WHO 2001 

NATIONAL 

Regulations and 

guidelines: 

a. Air 

ACGIH	 TLV–TWAb 0.2 mg/m3 ACGIH 2000 

NIOSH	 RELb 0.2 mg/m3 NIOSH 2001 

OSHA	 PEL (8-hour TWA)b 0.2 mg/m3 OSHA 2001 

b. Water 

EPA	 1-Day health advisory (10-kg child) 0.3 mg/L EPA 2000a 

10-Day health advisory (10-kg child) 0.3 mg/L 

Lifetime health advisory 2x10-3 mg/L 

DWEL	 9x10-3 mg/L 

c. Food 

EPA	 Revocation of tolerances for fruits EPA 1999e 

and vegetables commonly eaten by 

children, and other vegetables 

Establishment/retention of EPA 2001 

tolerances for residues in or on raw 

agricultural commodities in food 

crops (ppm) 

Almonds 0.1 

Apricots 1.0 

Avocados 1.0 

Barley 1.0 

Beans (dried) 1.0 

Beets (sugar), including tops 0.1 

Blackberries 1.0 

Blueberries 1.0 

Boysenberries 1.0 

Cabbage 1.0 

Clover 1.0 

Corn 1.0 
METHYL PARATHION 167 

8. REGULATIONS AND ADVISORIES 

Table 8-1. Regulations and Guidelines Applicable to Methyl Parathion 

(continued) 

Agency Description Information References 

NATIONAL (cont.) 

EPA (cont.) Establishment/retention of 

tolerances for residues in or on raw 

agricultural commodities in food 

crops (ppm) 

Cottonseed 

Cranberries 

Cucumbers 

Currants 

Dates 

Dewberries 

Eggplants 

Endive (escarole) 

Figs 

Filberts 

Garlic 

Gooseberries 

Guavas 

Hops 

Mangoes 

Melons 

Mustard seed 

Oats 

Okra 

Olives 

Onions 

Parsley 

Parsnips 

Parsnip greens 

Peanuts 

Peas (dried) 

Pecans 

Peppers 

Pineapple 

Potatoes 

Pumpkins 

Quinces 

Radishes (with or without tops) 

Rape (canola) seed 

Raspberries 

Rice 

Safflower seed 

Sorghum 

Soybeans 

Squash 

Strawberries 

EPA 2001
 

0.75 

1.0 

1.0 

1.0 

1.0 

1.0 

1.0 

1.0 

1.0 

0.1 

1.0 

1.0 

1.0 

1.0 

1.0 

1.0 

0.2 

1.0 

1.0 

1.0 

1.0 

1.0 

1.0 

1.0 

1.0 

1.0 

0.1 

1.0 

1.0 

0.1 

1.0 

1.0 

1.0 

0.2 

1.0 

1.0 

0.1 

0.1 

0.1 

1.0 

1.0 
METHYL PARATHION 168 

8. REGULATIONS AND ADVISORIES 

Table 8-1. Regulations and Guidelines Applicable to Methyl Parathion 

(continued) 

Agency Description	 Information References 

NATIONAL (cont.) 

EPA (cont.)	 Establishment/retention of EPA 2001 

tolerances for residues in or on raw 

agricultural commodities in food 

crops (ppm) 

Summer squash 1.0 

Sunflower seeds 0.2 

Sweet potatoes 0.1 

Swiss chard 1.0 

Walnuts 0.1 

Wheat 1.0 

Youngberries 1.0 

d. Other 

ACGIH	 Carcinogenic classification A4c ACGIH 2000 

EPA RfD	 2.5x10-4 IRIS 2001 

mg/kg/day 

Carcinogenic classification Group Dd	 EPA 2000a 

Designated hazardous substance in EPA 2000b 

accordance with Section 40CFR116.4 

311(b)(2)(a) 

Pesticide chemicals manufacturing EPA 2000c 

discharges 40CFR455.20 

RCRA—identification and listing as P071 EPA 2000d 

a hazardous waste 40CFR261.33 

CERCLA—reportable quantity 100 pounds	 EPA 1999f 

40CFR302.4 

Toxic chemical release reporting; 01/01/95 EPA 1999g 

Community Right-to-Know 40CFR372.65 

—effective date 

STATE 

Regulations and 

guidelines: 

a. Air: 

Arkansas Hazardous Air Pollutant	 ADEQ 2001 

RAC 0.3 μg/m3	 BNA 2001 

California RAC	 0.3 μg/m3 BNA 2001 
METHYL PARATHION 169 

8. REGULATIONS AND ADVISORIES 

Table 8-1. Regulations and Guidelines Applicable to Methyl Parathion 

(continued) 

Agency Description Information References 

STATE (cont.) 

California Toxic Air Contaminant California EPA 2001
 

Colorado Hazardous air pollutant BNA 2001
 

8 hour 4 μg/m3
 

30 minutes 20 μg/m3
 

Delaware RAC 0.3 μg/m3 BNA 2001
 

Idaho Toxic air pollutants BNA 2001
 

OEL 0.2 mg/m3
 

EL 0.013
 

pounds/hour 

AAC 0.01 mg/m3 

Illinois RAC 0.3 μg/m3 BNA 2001
 

Kentucky RAC 0.3 μg/m3 BNA 2001
 

New Hampshire Regulated toxic air contaminant BNA 2001
 

OEL 0.2 mg/m3
 

South Carolina RAC 0.3 μg/m3 BNA 2001
 

Tennessee RAC 0.3 μg/m3 BNA 2001
 

Wisconsin Proposed threshold Wisconsin DNR
 

24 hour<25 feet (pounds/hour) 0.0107 2001
 

24 hour$25 feet<75 feet 0.0417 

(pounds/hour)
 

24 hour$75 feet (pounds/hour) 0.324 

AAC 4.8 μg/L
 

Wyoming RAC 0.3 μg/m3 BNA 2001
 

b. Water:
 

Arizona Drinking water guideline 1.8 μg/L HSDB 2001
 

California Drinking water guideline 30 μg/L HSDB 2001
 

Florida Drinking water guideline 10 μg/L HSDB 2001
 

Kentucky Hazardous constituent for BNA 2001
 

groundwater monitoring
 

Maine Drinking water guideline 2 μg/L HSDB 2001
 
METHYL PARATHION 170 

8. REGULATIONS AND ADVISORIES 

Table 8-1. Regulations and Guidelines Applicable to Methyl Parathion 

(continued) 

Agency Description	 Information References 

STATE (cont.) 

Vermont	 Enforcement standard 2.0 μg/L BNA 2001 

Preventive action level 1.0 μg/L 

c. Food:	 No data 

d. Other: 

Arizona Soil remediation level BNA 2001 

Residential 16.0 mg/kg 

Non-residential 170 mg/kg 

Massachusetts RfD 2.5x10-4 BNA 2001 

mg/kg/day 

Missouri Hazardous constituent BNA 2001 

New Jersey Requires field posting CDC 2001 

Ohio Extremely hazardous substance Ohio EPA 2001 

a

Group 3: not classifiable as to its carcinogenicity to humans

b

Skin notation: danger of cutaneous absorption c

A4: not classifiable as a human carcinogen

d

Group D: inadequate or no human or animal evidence of carcinogenicity 

AAC = acceptable ambient concentration; ACGIH = American Conference of Governmental Industrial Hygienists; 

ADEQ = Arizona Department of Environmental Quality; BNA = Bureau of National Affairs; CDC = Center for Disease 

Control; CERCLA = Comprehensive Environmental Response, Compensation, and Liability Act; CFR = Code of 

Federal Regulations; DNR = Department of Natural Resources; DWEL = drinking water equivalent level; 

EL = emissions level; EPA = Environmental Protection Agency; HSDB = Hazardous Substances Data Bank; 

IARC = International Agency for Research on Cancer; IRIS = Integrated Risk Information System; NIOSH = National 

Institute of Occupational Safety and Health; OEL = occupational exposure limit; OSHA = Occupational Safety and 

Health Administration; PEL = permissible exposure limit; RAC = reference air concentration; REL = recommended 

exposure limit; RCRA = Resource Conservation and Recovery Act; RfD = reference dose; TLV = threshold limit value; 

TWA = time-weighted average; WHO = World Health Organization 
METHYL PARATHION 171 

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METHYL PARATHION 216 

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METHYL PARATHION 221 

10. GLOSSARY 

Absorption—The taking up of liquids by solids, or of gases by solids or liquids. 

Acute Exposure—Exposure to a chemical for a duration of 14 days or less, as specified in the 

Toxicological Profiles. 

Adsorption—The adhesion in an extremely thin layer of molecules (as of gases, solutes, or liquids) to the 

surfaces of solid bodies or liquids with which they are in contact. 

Adsorption Coefficient (Koc)—The ratio of the amount of a chemical adsorbed per unit weight of organic 

carbon in the soil or sediment to the concentration of the chemical in solution at equilibrium. 

Adsorption Ratio (Kd)—The amount of a chemical adsorbed by a sediment or soil (i.e., the solid phase) 

divided by the amount of chemical in the solution phase, which is in equilibrium with the solid phase, at a 

fixed solid/solution ratio. It is generally expressed in micrograms of chemical sorbed per gram of soil or 

sediment. 

Benchmark Dose (BMD)—Usually defined as the lower confidence limit on the dose that produces a 

specified magnitude of changes in a specified adverse response. For example, a BMD10 would be the 

dose at the 95% lower confidence limit on a 10% response, and the benchmark response (BMR) would be 

10%. The BMD is determined by modeling the dose response curve in the region of the dose response 

relationship where biologically observable data are feasible. 

Benchmark Dose Model—A statistical dose-response model applied to either experimental toxicological 

or epidemiological data to calculate a BMD. 

Bioconcentration Factor (BCF)—The quotient of the concentration of a chemical in aquatic organisms at 

a specific time or during a discrete time period of exposure divided by the concentration in the 

surrounding water at the same time or during the same period. 

Biomarkers—Broadly defined as indicators signaling events in biologic systems or samples. They have 

been classified as markers of exposure, markers of effect, and markers of susceptibility. 

Cancer Effect Level (CEL)—The lowest dose of chemical in a study, or group of studies, that produces 

significant increases in the incidence of cancer (or tumors) between the exposed population and its 

appropriate control. 

Carcinogen—A chemical capable of inducing cancer. 

Case-Control Study—A type of epidemiological study which examines the relationship between a 

particular outcome (disease or condition) and a variety of potential causative agents (such as toxic 

chemicals). In a case-controlled study, a group of people with a specified and well-defined outcome is 

identified and compared to a similar group of people without outcome. 

Case Report—Describes a single individual with a particular disease or exposure. These may suggest 

some potential topics for scientific research but are not actual research studies. 
METHYL PARATHION 222 

10. GLOSSARY 

Case Series—Describes the experience of a small number of individuals with the same disease or 

exposure. These may suggest potential topics for scientific research but are not actual research studies. 

Ceiling Value—A concentration of a substance that should not be exceeded, even instantaneously. 

Chronic Exposure—Exposure to a chemical for 365 days or more, as specified in the Toxicological 

Profiles. 

Cohort Study—A type of epidemiological study of a specific group or groups of people who have had a 

common insult (e.g., exposure to an agent suspected of causing disease or a common disease) and are 

followed forward from exposure to outcome. At least one exposed group is compared to one unexposed 

group. 

Cross-sectional Study—A type of epidemiological study of a group or groups which examines the 

relationship between exposure and outcome to a chemical or to chemicals at one point in time. 

Data Needs—Substance-specific informational needs that if met would reduce the uncertainties of human 

health assessment. 

Developmental Toxicity—The occurrence of adverse effects on the developing organism that may result 

from exposure to a chemical prior to conception (either parent), during prenatal development, or 

postnatally to the time of sexual maturation. Adverse developmental effects may be detected at any point 

in the life span of the organism. 

Dose-Response Relationship—The quantitative relationship between the amount of exposure to a 

toxicant and the incidence of the adverse effects. 

Embryotoxicity and Fetotoxicity—Any toxic effect on the conceptus as a result of prenatal exposure to a 

chemical; the distinguishing feature between the two terms is the stage of development during which the 

insult occurs. The terms, as used here, include malformations and variations, altered growth, and in utero 

death. 

Environmental Protection Agency (EPA) Health Advisory—An estimate of acceptable drinking water 

levels for a chemical substance based on health effects information. A health advisory is not a legally 

enforceable federal standard, but serves as technical guidance to assist federal, state, and local officials. 

Epidemiology—Refers to the investigation of factors that determine the frequency and distribution of 

disease or other health-related conditions within a defined human population during a specified period. 

Genotoxicity—A specific adverse effect on the genome of living cells that, upon the duplication of 

affected cells, can be expressed as a mutagenic, clastogenic or carcinogenic event because of specific 

alteration of the molecular structure of the genome. 

Half-life—A measure of rate for the time required to eliminate one half of a quantity of a chemical from 

the body or environmental media. 

Immediately Dangerous to Life or Health (IDLH)—The maximum environmental concentration of a 

contaminant from which one could escape within 30 minutes without any escape-impairing symptoms or 

irreversible health effects. 
METHYL PARATHION 223 

10. GLOSSARY 

Incidence—The ratio of individuals in a population who develop a specified condition to the total number 

of individuals in that population who could have developed that condition in a specified time period. 

Intermediate Exposure—Exposure to a chemical for a duration of 15–364 days, as specified in the 

Toxicological Profiles. 

Immunologic Toxicity—The occurrence of adverse effects on the immune system that may result from 

exposure to environmental agents such as chemicals. 

Immunological Effects—Functional changes in the immune response. 

In Vitro—Isolated from the living organism and artificially maintained, as in a test tube. 

In Vivo—Occurring within the living organism. 

Lethal Concentration(LO) (LCLO)—The lowest concentration of a chemical in air which has been reported 

to have caused death in humans or animals. 

Lethal Concentration(50) (LC50)—A calculated concentration of a chemical in air to which exposure for a 

specific length of time is expected to cause death in 50% of a defined experimental animal population. 

Lethal Dose(LO) (LDLO)—The lowest dose of a chemical introduced by a route other than inhalation that 

has been reported to have caused death in humans or animals. 

Lethal Dose(50) (LD50)—The dose of a chemical which has been calculated to cause death in 50% of a 

defined experimental animal population. 

Lethal Time(50) (LT50)—A calculated period of time within which a specific concentration of a chemical is 

expected to cause death in 50% of a defined experimental animal population. 

Lowest-Observed-Adverse-Effect Level (LOAEL)—The lowest exposure level of chemical in a study, or 

group of studies, that produces statistically or biologically significant increases in frequency or severity of 

adverse effects between the exposed population and its appropriate control. 

Lymphoreticular Effects—Represent morphological effects involving lymphatic tissues such as the 

lymph nodes, spleen, and thymus. 

Malformations—Permanent structural changes that may adversely affect survival, development, or 

function. 

Minimal Risk Level (MRL)—An estimate of daily human exposure to a hazardous substance that is 

likely to be without an appreciable risk of adverse noncancer health effects over a specified route and 

duration of exposure. 

Modifying Factor (MF)—A value (greater than zero) that is applied to the derivation of a minimal risk 

level (MRL) to reflect additional concerns about the database that are not covered by the uncertainty 

factors. The default value for a MF is 1. 

Morbidity—State of being diseased; morbidity rate is the incidence or prevalence of disease in a specific 

population. 
METHYL PARATHION 224 

10. GLOSSARY 

Mortality—Death; mortality rate is a measure of the number of deaths in a population during a specified 

interval of time. 

Mutagen—A substance that causes mutations. A mutation is a change in the DNA sequence of a cell’s 

DNA. Mutations can lead to birth defects, miscarriages, or cancer. 

Necropsy—The gross examination of the organs and tissues of a dead body to determine the cause of 

death or pathological conditions. 

Neurotoxicity—The occurrence of adverse effects on the nervous system following exposure to a 

chemical. 

No-Observed-Adverse-Effect Level (NOAEL)—The dose of a chemical at which there were no 

statistically or biologically significant increases in frequency or severity of adverse effects seen between 

the exposed population and its appropriate control. Effects may be produced at this dose, but they are not 

considered to be adverse. 

Octanol-Water Partition Coefficient (Kow)—The equilibrium ratio of the concentrations of a chemical in 

n-octanol and water, in dilute solution. 

Odds Ratio (OR)—A means of measuring the association between an exposure (such as toxic substances 

and a disease or condition) which represents the best estimate of relative risk (risk as a ratio of the 

incidence among subjects exposed to a particular risk factor divided by the incidence among subjects who 

were not exposed to the risk factor). An odds ratio of greater than 1 is considered to indicate greater risk 

of disease in the exposed group compared to the unexposed. 

Organophosphate or Organophosphorus Compound—A phosphorus containing organic compound and 

especially a pesticide that acts by inhibiting cholinesterase. 

Permissible Exposure Limit (PEL)—An Occupational Safety and Health Administration (OSHA) 

allowable exposure level in workplace air averaged over an 8-hour shift of a 40-hour workweek. 

Pesticide—General classification of chemicals specifically developed and produced for use in the control 

of agricultural and public health pests. 

Pharmacokinetics—The science of quantitatively predicting the fate (disposition) of an exogenous 

substance in an organism. Utilizing computational techniques, it provides the means of studying the 

absorption, distribution, metabolism and excretion of chemicals by the body. 

Pharmacokinetic Model—A set of equations that can be used to describe the time course of a parent 

chemical or metabolite in an animal system. There are two types of pharmacokinetic models: data-based 

and physiologically-based. A data-based model divides the animal system into a series of compartments 

which, in general, do not represent real, identifiable anatomic regions of the body whereby the 

physiologically-based model compartments represent real anatomic regions of the body. 

Physiologically Based Pharmacodynamic (PBPD) Model—A type of physiologically-based doseresponse model which quantitatively describes the relationship between target tissue dose and toxic end 

points. These models advance the importance of physiologically based models in that they clearly 

describe the biological effect (response) produced by the system following exposure to an exogenous 

substance. 
METHYL PARATHION 225 

10. GLOSSARY 

Physiologically Based Pharmacokinetic (PBPK) Model—Comprised of a series of compartments 

representing organs or tissue groups with realistic weights and blood flows. These models require a 

variety of physiological information: tissue volumes, blood flow rates to tissues, cardiac output, alveolar 

ventilation rates and, possibly membrane permeabilities. The models also utilize biochemical information 

such as air/blood partition coefficients, and metabolic parameters. PBPK models are also called 

biologically based tissue dosimetry models. 

Prevalence—The number of cases of a disease or condition in a population at one point in time. 

Prospective Study—A type of cohort study in which the pertinent observations are made on events 

occurring after the start of the study. A group is followed over time. 

q1

*—The upper-bound estimate of the low-dose slope of the dose-response curve as determined by the 

multistage procedure. The q1* can be used to calculate an estimate of carcinogenic potency, the 

incremental excess cancer risk per unit of exposure (usually μg/L for water, mg/kg/day for food, and 

μg/m3

 for air). 

Recommended Exposure Limit (REL)—A National Institute for Occupational Safety and Health 

(NIOSH) time-weighted average (TWA) concentrations for up to a 10-hour workday during a 40-hour 

workweek. 

Reference Concentration (RfC)—An estimate (with uncertainty spanning perhaps an order of magnitude) 

of a continuous inhalation exposure to the human population (including sensitive subgroups) that is likely 

to be without an appreciable risk of deleterious noncancer health effects during a lifetime. The inhalation 

reference concentration is for continuous inhalation exposures and is appropriately expressed in units of 

mg/m3 or ppm. 

Reference Dose (RfD)—An estimate (with uncertainty spanning perhaps an order of magnitude) of the 

daily exposure of the human population to a potential hazard that is likely to be without risk of deleterious 

effects during a lifetime. The RfD is operationally derived from the no-observed-adverse-effect level 

(NOAEL-from animal and human studies) by a consistent application of uncertainty factors that reflect 

various types of data used to estimate RfDs and an additional modifying factor, which is based on a 

professional judgment of the entire database on the chemical. The RfDs are not applicable to 

nonthreshold effects such as cancer. 

Reportable Quantity (RQ)—The quantity of a hazardous substance that is considered reportable under the 

Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA). Reportable 

quantities are (1) 1 pound or greater or (2) for selected substances, an amount established by regulation 

either under CERCLA or under Section 311 of the Clean Water Act. Quantities are measured over a 

24-hour period. 

Reproductive Toxicity—The occurrence of adverse effects on the reproductive system that may result 

from exposure to a chemical. The toxicity may be directed to the reproductive organs and/or the related 

endocrine system. The manifestation of such toxicity may be noted as alterations in sexual behavior, 

fertility, pregnancy outcomes, or modifications in other functions that are dependent on the integrity of 

this system. 

Retrospective Study—A type of cohort study based on a group of persons known to have been exposed at 

some time in the past. Data are collected from routinely recorded events, up to the time the study is 

undertaken. Retrospective studies are limited to causal factors that can be ascertained from existing 

records and/or examining survivors of the cohort. 
METHYL PARATHION 226 

10. GLOSSARY 

Risk—The possibility or chance that some adverse effect will result from a given exposure to a chemical. 

Risk Factor—An aspect of personal behavior or lifestyle, an environmental exposure, or an inborn or 

inherited characteristic, that is associated with an increased occurrence of disease or other health-related 

event or condition. 

Risk Ratio—The ratio of the risk among persons with specific risk factors compared to the risk among 

persons without risk factors. A risk ratio greater than 1 indicates greater risk of disease in the exposed 

group compared to the unexposed. 

Short-Term Exposure Limit (STEL)—The American Conference of Governmental Industrial Hygienists 

(ACGIH) maximum concentration to which workers can be exposed for up to 15 min continually. No 

more than four excursions are allowed per day, and there must be at least 60 min between exposure 

periods. The daily Threshold Limit Value - Time Weighted Average (TLV-TWA) may not be exceeded. 

Target Organ Toxicity—This term covers a broad range of adverse effects on target organs or 

physiological systems (e.g., renal, cardiovascular) extending from those arising through a single limited 

exposure to those assumed over a lifetime of exposure to a chemical. 

Teratogen—A chemical that causes structural defects that affect the development of an organism. 

Threshold Limit Value (TLV)—An American Conference of Governmental Industrial Hygienists 

(ACGIH) concentration of a substance to which most workers can be exposed without adverse effect. 

The TLV may be expressed as a Time Weighted Average (TWA), as a Short-Term Exposure Limit 

(STEL), or as a ceiling limit (CL). 

Time-Weighted Average (TWA)—An allowable exposure concentration averaged over a normal 8-hour 

workday or 40-hour workweek. 

Toxic Dose(50) (TD50)—A calculated dose of a chemical, introduced by a route other than inhalation, 

which is expected to cause a specific toxic effect in 50% of a defined experimental animal population. 

Toxicokinetic—The study of the absorption, distribution and elimination of toxic compounds in the 

living organism. 

Uncertainty Factor (UF)—A factor used in operationally deriving the Minimal Risk Level (MRL) or 

Reference Dose (RfD) or Reference Concentration (RfC) from experimental data. UFs are intended to 

account for (1) the variation in sensitivity among the members of the human population, (2) the 

uncertainty in extrapolating animal data to the case of human, (3) the uncertainty in extrapolating from 

data obtained in a study that is of less than lifetime exposure, and (4) the uncertainty in using lowestobserved-adverse-effect level (LOAEL) data rather than no-observed-adverse-effect level (NOAEL) data. 

A default for each individual UF is 10; if complete certainty in data exists, a value of one can be used; 

however a reduced UF of three may be used on a case-by-case basis, three being the approximate 

logarithmic average of 10 and 1. 

Xenobiotic—Any chemical that is foreign to the biological system. 
METHYL PARATHION A-1 

APPENDIX A
 

ATSDR MINIMAL RISK LEVEL AND WORKSHEETS
 

The Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA) [42 U.S.C. 

9601 et seq.], as amended by the Superfund Amendments and Reauthorization Act (SARA) [Pub. L. 

99–499], requires that the Agency for Toxic Substances and Disease Registry (ATSDR) develop jointly 

with the U.S. Environmental Protection Agency (EPA), in order of priority, a list of hazardous substances 

most commonly found at facilities on the CERCLA National Priorities List (NPL); prepare toxicological 

profiles for each substance included on the priority list of hazardous substances; and assure the initiation 

of a research program to fill identified data needs associated with the substances. 

The toxicological profiles include an examination, summary, and interpretation of available toxicological 

information and epidemiologic evaluations of a hazardous substance. During the development of 

toxicological profiles, Minimal Risk Levels (MRLs) are derived when reliable and sufficient data exist to 

identify the target organ(s) of effect or the most sensitive health effect(s) for a specific duration for a 

given route of exposure. An MRL is an estimate of the daily human exposure to a hazardous substance 

that is likely to be without appreciable risk of adverse noncancer health effects over a specified duration 

of exposure. MRLs are based on noncancer health effects only and are not based on a consideration of 

cancer effects. These substance-specific estimates, which are intended to serve as screening levels, are 

used by ATSDR health assessors to identify contaminants and potential health effects that may be of 

concern at hazardous waste sites. It is important to note that MRLs are not intended to define clean-up or 

action levels. 

MRLs are derived for hazardous substances using the no-observed-adverse-effect level/uncertainty factor 

approach. They are below levels that might cause adverse health effects in the people most sensitive to 

such chemical-induced effects. MRLs are derived for acute (1–14 days), intermediate (15–364 days), and 

chronic (365 days and longer) durations and for the oral and inhalation routes of exposure. Currently, 

MRLs for the dermal route of exposure are not derived because ATSDR has not yet identified a method 

suitable for this route of exposure. MRLs are generally based on the most sensitive chemical-induced end 

point considered to be of relevance to humans. Serious health effects (such as irreparable damage to the 

liver or kidneys, or birth defects) are not used as a basis for establishing MRLs. Exposure to a level 

above the MRL does not mean that adverse health effects will occur. 
METHYL PARATHION A-2 

APPENDIX A 

MRLs are intended only to serve as a screening tool to help public health professionals decide where to 

look more closely. They may also be viewed as a mechanism to identify those hazardous waste sites that 

are not expected to cause adverse health effects. Most MRLs contain a degree of uncertainty because of 

the lack of precise toxicological information on the people who might be most sensitive (e.g., infants, 

elderly, nutritionally or immunologically compromised) to the effects of hazardous substances. ATSDR 

uses a conservative (i.e., protective) approach to address this uncertainty consistent with the public health 

principle of prevention. Although human data are preferred, MRLs often must be based on animal studies 

because relevant human studies are lacking. In the absence of evidence to the contrary, ATSDR assumes 

that humans are more sensitive to the effects of hazardous substance than animals and that certain persons 

may be particularly sensitive. Thus, the resulting MRL may be as much as a hundredfold below levels 

that have been shown to be nontoxic in laboratory animals. 

Proposed MRLs undergo a rigorous review process: Health Effects/MRL Workgroup reviews within the 

Division of Toxicology, expert panel peer reviews, and agencywide MRL Workgroup reviews, with 

participation from other federal agencies and comments from the public. They are subject to change as 

new information becomes available concomitant with updating the toxicological profiles. Thus, MRLs in 

the most recent toxicological profiles supersede previously published levels. For additional information 

regarding MRLs, please contact the Division of Toxicology, Agency for Toxic Substances and Disease 

Registry, 1600 Clifton Road, Mailstop E-29, Atlanta, Georgia 30333. 
METHYL PARATHION A-3 

APPENDIX A 

MINIMAL RISK LEVEL (MRL) WORKSHEET 

Chemical Name: Methyl parathion 

CAS Number: 298-00-0 

Date: June 22, 2001 

Profile Status: Final 

Route: [ ] Inhalation [X] Oral 

Duration: [ ] Acute [X] Intermediate [ ] Chronic 

Key to Figure: 32 

Species: Rats 

Minimal Risk Level: 0.0007 [X] mg/kg/day [ ] mg/m3 

Reference: Desi I, Nagymajtenyi L, Papp A, et al. 1998. Experimental model studies of pesticide 

exposure. Neurotoxicology 19:611-616. 

Experimental design (human study details or strain, number of animals per exposure/control groups, sex, 

dose administration details): Male rats were treated with methyl parathion in an aqueous vehicle through 

gavage administration to their dams during days 5–15 of gestation and days 2–28 of lactation at doses of 

0.22, 0.44, or 0.88 mg/kg/day, followed by direct treatment of the male offspring in the same manner for 

8 weeks, from weaning through 11–12 weeks of age. Electrophysiological testing was performed on the 

male offspring at the end of the treatment period. 

Effects noted in study and corresponding concentrations: Dose-related changes on electrocorticograms of 

the somatosensory, visual, and auditory centers, on evoked potentials, and on tail nerve conduction 

velocity and refractory period were observed in the male offspring (Desi et al. 1998). The results were 

stated to be significantly different from controls at all three dose levels, but results specifically for methyl 

parathion were shown only for the electrocorticograms of the somatosensory area. No overt signs of 

toxicity or effects on body weight were seen in the male offspring. 

In the same study (Desi et al. 1998), no significant effects on these end points were seen in male rats 

exposed to methyl parathion only through the treatment of their dams during gestation or during gestation 

and lactation, and then maintained without treatment until testing at 11–12 weeks of age. 

Concentration and end point used for MRL derivation: 0.22 mg/kg/day; electrophysiological effects in 

the central and peripheral nervous systems 

[ ] NOAEL [X] LOAEL 

Uncertainty Factors used in MRL derivation: 

[X] 3 for use of a minimal LOAEL 

[X] 10 for extrapolation from animals to humans 

[X] 10 for human variability 

Was a conversion factor used from ppm in food or water to a mg/body weight dose? No. 
METHYL PARATHION A-4 

APPENDIX A 

If an inhalation study in animals, list conversion factors used in determining human equivalent 

concentration: NA 

Was a conversion used from intermittent to continuous exposure? NA 

Other additional studies or pertinent information that lend support to this MRL: Methyl parathion affects 

the nervous system by inhibiting acetylcholinesterase activity. Cholinesterase inhibition and neurological 

effects have been observed in humans and animals, for all exposure routes and durations (for example, 

Dean et al. 1984; Desi et al. 1998; EPA 1978e; Gupta et al. 1985; Nemec et al. 1968; Suba 1984). 

Agency Contact (Chemical Manager): Jewell D. Wilson, Ph.D. 
METHYL PARATHION A-5 

APPENDIX A 

MINIMAL RISK LEVEL (MRL) WORKSHEET 

Chemical Name: Methyl parathion 

CAS Number: 298-00-0 

Date: June 22, 2001 

Profile Status: Final 

Route: [ ] Inhalation [X] Oral 

Duration: [ ] Acute [ ] Intermediate [X] Chronic 

Key to Figure: 38 

Species: Rats 

Minimal Risk Level: 0.0003 [X] mg/kg/day [ ] mg/m3 

Reference: Suba, LA. 1984. Additional information to support the registration of methyl parathion: 

Two year chronic feeding study of methyl parathion in rats. St. Louis, MO: Monsanto Agricultural 

Products Company. 

Experimental design (human study details or strain, number of animals per exposure/control groups, sex, 

dose administration details): Sprague-Dawley CD rats (60/sex/dose) were fed methyl parathion at dietary 

concentrations of 0, 0.5, 5, or 50 ppm (0, 0.025, 0.25, or 2.5 mg/kg/day) for 26 months (males) or 

28 months (females). Animals were observed twice daily for clinical signs and weighed weekly. 

Hematological and clinical chemistry, and urinalysis determinations were performed at 6, 12, 18, and 24 

months and at study termination. Five rats/sex/group were killed at approximately 24 months for 

examination of the brain, spinal cord and sciatic nerves. Complete necropsies and histopathological 

examinations of a wide range of organs and tissues were performed. 

Effects noted in study and corresponding concentrations: No adverse effects were observed in the lowdose male and female rats. Mean hemoglobin, hematocrit, and erythrocyte counts were significantly 

reduced in the high-dose females at 6–24 months of treatment; mean hematocrit and erythrocyte counts 

were significantly reduced in the mid- and high-dose males at 24 months of treatment. 

Abnormal gait involving the hind legs was observed in 1 mid-dose female from week 77 until 

termination, in 4–14 of the high-dose female rats from week 19 to termination, and in 1 high-dose male 

around the beginning of the second year. Slight tremor was noted during the first 3 weeks to 4 months of 

treatment in both sexes of the high-dose group. Peripheral neuropathy of the proximal and distal sciatic 

nerve was considered to be related to exposure to methyl parathion at the high dose. Methyl parathion 

did not induce histopathological effects in the brain or spinal cord. Statistical significance was not 

reported for these clinical signs and histopathological effects. Mean plasma, erythrocyte, and brain 

cholinesterase activities were significantly reduced by 67–88, 9–20, and 76–79%, respectively, in rats of 

both sexes following 2-year exposures only at the high dose of methyl parathion. 

Additional effects, which occurred only at the high dose, were retinal degeneration or atrophy and 

posterior subcapsular cataracts in the females. Slightly reduced body weights occurred in both sexes at 

the high dose at 2 years, but not consistently throughout the study, and food consumption was slightly 

elevated in the high-dose females. 
METHYL PARATHION A-6 

APPENDIX A 

Concentration and end point used for MRL derivation: 0.025 mg/kg/day; decreased mean hematocrit and 

erythrocyte counts 

[X] NOAEL [ ] LOAEL 

Uncertainty Factors used in MRL derivation: 

[ ] 10 for use of a LOAEL 

[X] 10 for extrapolation from animals to humans 

[X] 10 for human variability 

Was a conversion factor used from ppm in food or water to a mg/body weight dose? Yes. A chronic 

food factor of 0.05 kg feed/kg body weight/day for rats was used to convert from ppm in food to mg/kg as 

follows: 0.5 ppm x 0.05 = 0.025 mg/kg/day. (Data regarding body weight and food consumption were 

not available.) This is the food factor used in the original MRL derivation. 

If an inhalation study in animals, list conversion factors used in determining human equivalent 

concentration: NA 

Was a conversion used from intermittent to continuous exposure? NA 

Other additional studies or pertinent information that lend support to this MRL: An intermediate-duration 

gavage study in rats found decreased hematocrit and erythrocyte counts relative to before-treatment 

values (Galal et al. 1977), but this study had some limitations, including lack of a control group and 

disparities between text and tables. Another intermediate duration gavage study in male rats 

demonstrated dose-related significant decreases in mean corpuscular volume (Undeger et al. 2000). An 

effect on the erythrocyte is plausible because erythrocyte cholinesterase has a function in the control of 

erythrocyte permeability (Wills 1972). 

Agency Contact (Chemical Manager): Jewell D. Wilson, Ph.D. 
METHYL PARATHION B-1 

APPENDIX B 

USER'S GUIDE 

Chapter 1 

Public Health Statement 

This chapter of the profile is a health effects summary written in non-technical language. Its intended 

audience is the general public especially people living in the vicinity of a hazardous waste site or 

chemical release. If the Public Health Statement were removed from the rest of the document, it would 

still communicate to the lay public essential information about the chemical. 

The major headings in the Public Health Statement are useful to find specific topics of concern. The 

topics are written in a question and answer format. The answer to each question includes a sentence that 

will direct the reader to chapters in the profile that will provide more information on the given topic. 

Chapter 2 

Relevance to Public Health 

This chapter provides a health effects summary based on evaluations of existing toxicologic, 

epidemiologic, and toxicokinetic information. This summary is designed to present interpretive, 

weight-of-evidence discussions for human health end points by addressing the following questions. 

1.	 What effects are known to occur in humans? 

2.	 What effects observed in animals are likely to be of concern to humans? 

3.	 What exposure conditions are likely to be of concern to humans, especially around hazardous 

waste sites? 

The chapter covers end points in the same order they appear within the Discussion of Health Effects by 

Route of Exposure section, by route (inhalation, oral, dermal) and within route by effect. Human data are 

presented first, then animal data. Both are organized by duration (acute, intermediate, chronic). In vitro 

data and data from parenteral routes (intramuscular, intravenous, subcutaneous, etc.) are also considered 

in this chapter. If data are located in the scientific literature, a table of genotoxicity information is 

included. 

The carcinogenic potential of the profiled substance is qualitatively evaluated, when appropriate, using 

existing toxicokinetic, genotoxic, and carcinogenic data. ATSDR does not currently assess cancer 

potency or perform cancer risk assessments. Minimal risk levels (MRLs) for noncancer end points (if 

derived) and the end points from which they were derived are indicated and discussed. 

Limitations to existing scientific literature that prevent a satisfactory evaluation of the relevance to public 

health are identified in the Chapter 3 Data Needs section. 
METHYL PARATHION B-2 

APPENDIX B 

Interpretation of Minimal Risk Levels 

Where sufficient toxicologic information is available, we have derived minimal risk levels (MRLs) for 

inhalation and oral routes of entry at each duration of exposure (acute, intermediate, and chronic). These 

MRLs are not meant to support regulatory action; but to acquaint health professionals with exposure 

levels at which adverse health effects are not expected to occur in humans. They should help physicians 

and public health officials determine the safety of a community living near a chemical emission, given the 

concentration of a contaminant in air or the estimated daily dose in water. MRLs are based largely on 

toxicological studies in animals and on reports of human occupational exposure. 

MRL users should be familiar with the toxicologic information on which the number is based. Chapter 2, 

"Relevance to Public Health," contains basic information known about the substance. Other sections such 

as Chapter 3 Section 3.9, "Interactions with Other Substances,” and Section 3.10, "Populations that are 

Unusually Susceptible" provide important supplemental information. 

MRL users should also understand the MRL derivation methodology. MRLs are derived using a 

modified version of the risk assessment methodology the Environmental Protection Agency (EPA) 

provides (Barnes and Dourson 1988) to determine reference doses for lifetime exposure (RfDs). 

To derive an MRL, ATSDR generally selects the most sensitive end point which, in its best judgement, 

represents the most sensitive human health effect for a given exposure route and duration. ATSDR 

cannot make this judgement or derive an MRL unless information (quantitative or qualitative) is available 

for all potential systemic, neurological, and developmental effects. If this information and reliable 

quantitative data on the chosen end point are available, ATSDR derives an MRL using the most sensitive 

species (when information from multiple species is available) with the highest NOAEL that does not 

exceed any adverse effect levels. When a NOAEL is not available, a lowest-observed-adverse-effect 

level (LOAEL) can be used to derive an MRL, and an uncertainty factor (UF) of 10 must be employed. 

Additional uncertainty factors of 10 must be used both for human variability to protect sensitive 

subpopulations (people who are most susceptible to the health effects caused by the substance) and for 

interspecies variability (extrapolation from animals to humans). In deriving an MRL, these individual 

uncertainty factors are multiplied together. The product is then divided into the inhalation concentration 

or oral dosage selected from the study. Uncertainty factors used in developing a substance-specific MRL 

are provided in the footnotes of the LSE Tables. 

Chapter 3 

Health Effects 

Tables and Figures for Levels of Significant Exposure (LSE) 

Tables (3-1, 3-2, and 3-3) and figures (3-1 and 3-2) are used to summarize health effects and illustrate 

graphically levels of exposure associated with those effects. These levels cover health effects observed at 

increasing dose concentrations and durations, differences in response by species, minimal risk levels 

(MRLs) to humans for noncancer end points, and EPA's estimated range associated with an upper- bound 

individual lifetime cancer risk of 1 in 10,000 to 1 in 10,000,000. Use the LSE tables and figures for a 

quick review of the health effects and to locate data for a specific exposure scenario. The LSE tables and 

figures should always be used in conjunction with the text. All entries in these tables and figures 

represent studies that provide reliable, quantitative estimates of No-Observed-Adverse-Effect Levels 

(NOAELs), Lowest-Observed-Adverse-Effect Levels (LOAELs), or Cancer Effect Levels (CELs). 
METHYL PARATHION B-3 

APPENDIX B 

The legends presented below demonstrate the application of these tables and figures. Representative 

examples of LSE Table 3-1 and Figure 3-1 are shown. The numbers in the left column of the legends 

correspond to the numbers in the example table and figure. 

LEGEND 

See LSE Table 3-1 

(1)	 Route of Exposure One of the first considerations when reviewing the toxicity of a substance using 

these tables and figures should be the relevant and appropriate route of exposure. When sufficient 

data exists, three LSE tables and two LSE figures are presented in the document. The three LSE 

tables present data on the three principal routes of exposure, i.e., inhalation, oral, and dermal (LSE 

Table 3-1, 3-2, and 3-3, respectively). LSE figures are limited to the inhalation (LSE Figure 3-1) 

and oral (LSE Figure 3-2) routes. Not all substances will have data on each route of exposure and 

will not therefore have all five of the tables and figures. 

(2)	 Exposure Period Three exposure periods - acute (less than 15 days), intermediate (15–364 days), 

and chronic (365 days or more) are presented within each relevant route of exposure. In this 

example, an inhalation study of intermediate exposure duration is reported. For quick reference to 

health effects occurring from a known length of exposure, locate the applicable exposure period 

within the LSE table and figure. 

(3)	 Health Effect The major categories of health effects included in LSE tables and figures are death, 

systemic, immunological, neurological, developmental, reproductive, and cancer. NOAELs and 

LOAELs can be reported in the tables and figures for all effects but cancer. Systemic effects are 

further defined in the "System" column of the LSE table (see key number 18). 

(4)	 Key to Figure Each key number in the LSE table links study information to one or more data points 

using the same key number in the corresponding LSE figure. In this example, the study represented 

by key number 18 has been used to derive a NOAEL and a Less Serious LOAEL (also see the 2 

"18r" data points in Figure 3-1). 

(5)	 Species The test species, whether animal or human, are identified in this column. Chapter 2, 

"Relevance to Public Health," covers the relevance of animal data to human toxicity and 

Section 3.4, "Toxicokinetics," contains any available information on comparative toxicokinetics. 

Although NOAELs and LOAELs are species specific, the levels are extrapolated to equivalent 

human doses to derive an MRL. 

(6)	 Exposure Frequency/Duration The duration of the study and the weekly and daily exposure 

regimen are provided in this column. This permits comparison of NOAELs and LOAELs from 

different studies. In this case (key number 18), rats were exposed to 1,1,2,2-tetrachloroethane via 

inhalation for 6 hours per day, 5 days per week, for 3 weeks. For a more complete review of the 

dosing regimen refer to the appropriate sections of the text or the original reference paper, i.e., 

Nitschke et al. 1981. 

(7)	 System This column further defines the systemic effects. These systems include: respiratory, 

cardiovascular, gastrointestinal, hematological, musculoskeletal, hepatic, renal, and dermal/ocular. 

"Other" refers to any systemic effect (e.g., a decrease in body weight) not covered in these systems. 

In the example of key number 18, 1 systemic effect (respiratory) was investigated. 
METHYL PARATHION B-4 

APPENDIX B 

(8)	 NOAEL A No-Observed-Adverse-Effect Level (NOAEL) is the highest exposure level at which no 

harmful effects were seen in the organ system studied. Key number 18 reports a NOAEL of 3 ppm 

for the respiratory system which was used to derive an intermediate exposure, inhalation MRL of 

0.005 ppm (see footnote "b"). 

(9)	 LOAEL A Lowest-Observed-Adverse-Effect Level (LOAEL) is the lowest dose used in the study 

that caused a harmful health effect. LOAELs have been classified into "Less Serious" and 

"Serious" effects. These distinctions help readers identify the levels of exposure at which adverse 

health effects first appear and the gradation of effects with increasing dose. A brief description of 

the specific end point used to quantify the adverse effect accompanies the LOAEL. The respiratory 

effect reported in key number 18 (hyperplasia) is a Less serious LOAEL of 10 ppm. MRLs are not 

derived from Serious LOAELs. 

(10)	 Reference The complete reference citation is given in Chapter 9 of the profile. 

(11)	 CEL A Cancer Effect Level (CEL) is the lowest exposure level associated with the onset of 

carcinogenesis in experimental or epidemiologic studies. CELs are always considered serious 

effects. The LSE tables and figures do not contain NOAELs for cancer, but the text may report 

doses not causing measurable cancer increases. 

(12)	 Footnotes Explanations of abbreviations or reference notes for data in the LSE tables are found in 

the footnotes. Footnote "b" indicates the NOAEL of 3 ppm in key number 18 was used to derive an 

MRL of 0.005 ppm. 

LEGEND 

See Figure 3-1 

LSE figures graphically illustrate the data presented in the corresponding LSE tables. Figures help the 

reader quickly compare health effects according to exposure concentrations for particular exposure 

periods. 

(13)	 Exposure Period The same exposure periods appear as in the LSE table. In this example, health 

effects observed within the intermediate and chronic exposure periods are illustrated. 

(14)	 Health Effect These are the categories of health effects for which reliable quantitative data exists. 

The same health effects appear in the LSE table. 

(15)	 Levels of Exposure concentrations or doses for each health effect in the LSE tables are graphically 

displayed in the LSE figures. Exposure concentration or dose is measured on the log scale "y" axis. 

Inhalation exposure is reported in mg/m3

 or ppm and oral exposure is reported in mg/kg/day. 

(16)	 NOAEL In this example, 18r NOAEL is the critical end point for which an intermediate inhalation 

exposure MRL is based. As you can see from the LSE figure key, the open-circle symbol indicates 

to a NOAEL for the test species-rat. The key number 18 corresponds to the entry in the LSE table. 

The dashed descending arrow indicates the extrapolation from the exposure level of 3 ppm (see 

entry 18 in the Table) to the MRL of 0.005 ppm (see footnote "b" in the LSE table). 

(17)	 CEL Key number 38r is 1 of 3 studies for which Cancer Effect Levels were derived. The diamond 

symbol refers to a Cancer Effect Level for the test species-mouse. The number 38 corresponds to 

the entry in the LSE table. 
METHYL PARATHION B-5 

APPENDIX B 

(18)	 Estimated Upper-Bound Human Cancer Risk Levels This is the range associated with the 

upper-bound for lifetime cancer risk of 1 in 10,000 to 1 in 10,000,000. These risk levels are 

derived from the EPA's Human Health Assessment Group's upper-bound estimates of the slope of 

the cancer dose response curve at low dose levels (q1*). 

(19)	 Key to LSE Figure The Key explains the abbreviations and symbols used in the figure. 
2 

SAMPLE 

6 Table 3-1. Levels of Significant Exposure to [Chemical x] – Inhalation 1 

3 4 

Key to figurea Species 

Exposure frequency/ duration System 

NOAEL (ppm) 

6 INTERMEDIATE EXPOSURE 

5 6 7 8 

6 Systemic 9 9 9 9

6 18 Rat 13 wk 

5 d/wk 6 hr/d 

Resp 3b 

CHRONIC EXPOSURE Cancer 38 Rat 18 mo 

5 d/wk 7 hr/d 

39 Rat 89–104 wk 

5 d/wk 6 hr/d 

40 Mouse 79–103 wk 

5 d/wk 6 hr/d 

a The number corresponds to entries in Figure 3-1. 

LOAEL (effect) 

Less serious (ppm) Serious (ppm) 

9 

9 

10 (hyperplasia) 

11 

9

20 (CEL, multiple 

organs) 

10 (CEL, lung tumors

nasal tumors) 

10 (CEL, lung tumors

hemangiosarcom

b Used to derive an intermediate inhalation Minimal Risk Level (MRL) of 5 x 10-3 ppm; dose adjusted for intermittent ex

an uncertainty factor of 100 (10 for extrapolation from animal to humans, 10 for human variability). 12 6

METHYL PARATHION C-1 

APPENDIX C 

ACRONYMS, ABBREVIATIONS, AND SYMBOLS 

ACGIH American Conference of Governmental Industrial Hygienists 

ADI Acceptable Daily Intake 

ADME Absorption, Distribution, Metabolism, and Excretion 

AFID alkali flame ionization detector 

AFOSH Air Force Office of Safety and Health 

AML acute myeloid leukemia 

AOAC Association of Official Analytical Chemists 

atm atmosphere 

ATSDR Agency for Toxic Substances and Disease Registry 

AWQC Ambient Water Quality Criteria 

BAT Best Available Technology 

BCF bioconcentration factor 

BEI Biological Exposure Index 

BSC Board of Scientific Counselors 

C Centigrade 

CAA Clean Air Act 

CAG Cancer Assessment Group of the U.S. Environmental Protection Agency 

CAS Chemical Abstract Services 

CDC Centers for Disease Control and Prevention 

CEL Cancer Effect Level 

CELDS Computer-Environmental Legislative Data System 

CERCLA Comprehensive Environmental Response, Compensation, and Liability Act 

CFR Code of Federal Regulations 

Ci curie 

CL ceiling limit value 

CLP Contract Laboratory Program 

cm centimeter 

CML chronic myeloid leukemia 

CNS central nervous system 

CPSC Consumer Products Safety Commission 

CWA Clean Water Act 

d day 

Derm dermal 

DHEW Department of Health, Education, and Welfare 

DHHS Department of Health and Human Services 

DNA deoxyribonucleic acid 

DOD Department of Defense 

DOE Department of Energy 

DOL Department of Labor 

DOT Department of Transportation 

DOT/UN/ Department of Transportation/United Nations/ 

NA/IMCO North America/International Maritime Dangerous Goods Code 

DWEL Drinking Water Exposure Level 

ECD electron capture detection 

ECG/EKG electrocardiogram 
 

METHYL PARATHION C-2 

APPENDIX C 

EEG electroencephalogram 

EEGL Emergency Exposure Guidance Level 

EPA Environmental Protection Agency 

F Fahrenheit 

F1 first-filial generation 

FAO Food and Agricultural Organization of the United Nations 

FDA Food and Drug Administration 

FEMA Federal Emergency Management Agency 

FIFRA Federal Insecticide, Fungicide, and Rodenticide Act 

FPD flame photometric detection 

fpm feet per minute 

ft foot 

FR Federal Register 

g gram 

GC gas chromatography 

Gd gestational day 

gen generation 

GLC gas liquid chromatography 

GPC gel permeation chromatography 

HPLC high-performance liquid chromatography 

hr hour 

HRGC high resolution gas chromatography 

HSDB Hazardous Substance Data Bank 

IDLH Immediately Dangerous to Life and Health 

IARC International Agency for Research on Cancer 

ILO International Labor Organization 

in inch 

IRIS Integrated Risk Information System 

Kd adsorption ratio 

kg kilogram 

kkg metric ton 

Koc organic carbon partition coefficient 

Kow octanol-water partition coefficient 

L liter 

LC liquid chromatography 

LCLo lethal concentration, low 

LC50 lethal concentration, 50% kill 

LDLo lethal dose, low 

LD50 lethal dose, 50% kill 

LT50 lethal time, 50% kill 

LOAEL lowest-observed-adverse-effect level 

LSE Levels of Significant Exposure 

m meter 

MA trans,trans-muconic acid 

MAL Maximum Allowable Level 

mCi millicurie 

MCL Maximum Contaminant Level 

MCLG Maximum Contaminant Level Goal 

mg milligram 

min minute 

mL milliliter 
METHYL PARATHION C-3 

APPENDIX C 

mm millimeter 

mm Hg millimeters of mercury 

mmol millimole 

mo month 

mppcf millions of particles per cubic foot 

MRL Minimal Risk Level 

MS mass spectrometry 

NAAQS National Ambient Air Quality Standard 

NAS National Academy of Science 

NATICH National Air Toxics Information Clearinghouse 

NATO North Atlantic Treaty Organization 

NCE normochromatic erythrocytes 

NCI National Cancer Institute 

NIEHS National Institute of Environmental Health Sciences 

NIOSH National Institute for Occupational Safety and Health 

NIOSHTIC NIOSH's Computerized Information Retrieval System 

NFPA National Fire Protection Association 

ng nanogram 

NLM National Library of Medicine 

nm nanometer 

NHANES National Health and Nutrition Examination Survey 

nmol nanomole 

NOAEL no-observed-adverse-effect level 

NOES National Occupational Exposure Survey 

NOHS National Occupational Hazard Survey 

NPD nitrogen phosphorus detection 

NPDES National Pollutant Discharge Elimination System 

NPL National Priorities List 

NR not reported 

NRC National Research Council 

NS not specified 

NSPS New Source Performance Standards 

NTIS National Technical Information Service 

NTP National Toxicology Program 

ODW Office of Drinking Water, EPA 

OERR Office of Emergency and Remedial Response, EPA 

OHM/TADS Oil and Hazardous Materials/Technical Assistance Data System 

OPP Office of Pesticide Programs, EPA 

OPPTS Office of Prevention, Pesticides and Toxic Substances, EPA 

OPPT Office of Pollution Prevention and Toxics, EPA 

OSHA Occupational Safety and Health Administration 

OSW Office of Solid Waste, EPA 

OTS Office of Toxic Substances 

OW Office of Water 

OWRS Office of Water Regulations and Standards, EPA 

PAH Polycyclic Aromatic Hydrocarbon 

PBPD Physiologically Based Pharmacodynamic 

PBPK Physiologically Based Pharmacokinetic 

PCE polychromatic erythrocytes 

PEL permissible exposure limit 

PID photo ionization detector 
METHYL PARATHION C-4 

APPENDIX C 

pg picogram 

pmol picomole 

PHS Public Health Service 

PMR proportionate mortality ratio 

ppb parts per billion 

ppm parts per million 

ppt parts per trillion 

PSNS Pretreatment Standards for New Sources 

REL recommended exposure level/limit 

RfC Reference Concentration 

RfD Reference Dose 

RNA ribonucleic acid 

RTECS Registry of Toxic Effects of Chemical Substances 

RQ Reportable Quantity 

SARA Superfund Amendments and Reauthorization Act 

SCE sister chromatid exchange 

sec second 

SIC Standard Industrial Classification 

SIM selected ion monitoring 

SMCL Secondary Maximum Contaminant Level 

SMR standard mortality ratio 

SNARL Suggested No Adverse Response Level 

SPEGL Short-Term Public Emergency Guidance Level 

STEL short term exposure limit 

STORET Storage and Retrieval 

TD50 toxic dose, 50% specific toxic effect 

TLV threshold limit value 

TOC Total Organic Compound 

TPQ Threshold Planning Quantity 

TRI Toxics Release Inventory 

TSCA Toxic Substances Control Act 

TRI Toxics Release Inventory 

TWA time-weighted average 

U.S. United States 

UF uncertainty factor 

VOC Volatile Organic Compound 

yr year 

WHO World Health Organization 

wk week 

> greater than 

> greater than or equal to 

= equal to 

< less than 

< less than or equal to 

% percent α alpha β beta γ gamma δ delta 

μm micrometer 
METHYL PARATHION C-5 

APPENDIX C 

μg microgram q1

* cancer slope factor 

– negative 

+ positive 

(+) weakly positive result 

(–) weakly negative result 
METHYL PARATHION D-1 

APPENDIX D
 

INDEX 

acetylcholine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10, 78, 79, 85, 92, 96, 154 
 

acetylcholinesterase . . . . . . . . . . . . . . . . . . . . . . . 10-13, 47, 48, 51, 57, 78, 79, 82, 83, 85-88, 91, 92, 94, 96, 102, 144, 148, 154
 

acute dermal exposure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 66 
 

acute inhalation exposure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65 
 

adsorption . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127-129
 

aerobic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 132 
 

alanine aminotransferase . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42 
 

ambient air . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 147 
 

atropine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 92, 96 
 

bass . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 138 
 

BCF . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 129, 130
 

bioaccumulation .................................................................................. 146-148
 

bioavailability ................................................................................... 146, 148
 

bioconcentration . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8, 122, 129, 130
 

biodegradation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8, 122, 127, 130-132
 

biomagnification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 130 
 

biomarker . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 88, 89, 91, 105, 147
 

birds . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83 
 

body weight effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44 
 

breast milk . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4, 9, 64, 67, 73, 87, 108, 141, 143, 148
 

butyrylcholinesterase . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79, 85 
 

cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3, 4, 24, 52, 57, 83, 85, 101, 104, 111, 167
 

carcinogen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 167 
 

carcinogenic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10, 16, 17, 24, 52, 53, 57, 163, 165
 

carcinogenicity .............................................................................. 101, 163, 167
 

cardiovascular effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12, 21, 40, 41, 55 
 

cholinesterase . . . . . . . . . . . . . . . . . . . 6, 10-13, 15, 18, 22-24, 26, 46-49, 56, 58, 64-66, 68, 69, 71, 72, 77, 79, 83, 85-87, 90-94, 
 

100, 101, 105, 144, 154, 160, 162
 

delayed neurotoxicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12, 80 
 

dermal effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21, 43, 55 
 

DNA . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61-63, 89, 102 
 

dog . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69, 152 
 

estrogenic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57, 82, 83 
 

FDA . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2-4, 6, 137-140, 142
 

FEDRIP . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 148 
 

fetus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4, 64, 68, 74, 84 
 

fiber . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 154, 155
 

Food and Drug Administration (see FDA) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2, 6, 137 
 

fruits . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5, 7, 9, 117, 137, 138, 162, 163
 

gastrointestinal effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41, 107 
 

general population . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5, 8, 9, 88, 93, 105, 122, 139-141, 143, 148
 

half-life . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 74, 89, 106, 107, 130-133, 147
 

hematological effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12, 15, 26, 41, 100, 101
 

Henry’s law . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112 
 

hepatic effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21, 22, 42, 43 
 

hydrolysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8, 10, 64, 69, 72, 77, 79, 86, 90, 122, 127, 130-132, 154
 

immune system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46 
 

immunological effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22, 45, 46, 55, 103 
 

insects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1, 3, 5, 116, 141, 144, 149
 

Integrated Risk Information System . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 167 
 

intermediate oral exposure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12 
 

intermediate syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11, 96 
 

kidney . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22, 25, 68, 94 
 

LD50 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25, 26, 40, 42, 53, 55-57, 72, 80, 86, 93 
 

lice . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 116 
 

liver . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3, 21, 25, 42, 64, 67-69, 71, 72, 74, 76, 77, 79, 87, 89, 90, 93, 94, 99 
 
METHYL PARATHION D-2 

APPENDIX D 

lung . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62, 63, 89 
 

lymph . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45 
 

lymphoreticular effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22, 45, 55 
 

mass spectroscopy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 155 
 

melanoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45 
 

methyl paraoxon . . . . . . . . . . . . . . . . . . . . 2, 3, 10, 25, 26, 64, 67-69, 71, 72, 77, 79, 86, 87, 92, 93, 106, 107, 127, 130, 132-134,
 

136, 138, 143, 146, 155, 160
 

milk . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4, 9, 64, 67, 73, 87, 108, 138, 141-143, 148
 

Monsanto . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 114 
 

mosquito . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 116, 145
 

MRL . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14, 15, 17, 42, 48, 99-101, 162
 

muscarinic receptors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48, 51, 79 
 

musculoskeletal effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42 
 

NAS/NRC . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 88, 89 
 

National Priorities List (see NPL) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1, 9, 122 
 

neurobehavioral . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46, 81, 100, 103
 

neurodevelopmental . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99 
 

neurotransmitter . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10, 79, 85 
 

nicotinic receptors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79 
 

NIOSH . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6, 7, 91, 105, 111, 114, 140, 152, 163, 167
 

nitrophenol . . . . . . . . . . . . . . . . . . . . . . . . . . 6, 18, 22, 64-66, 69, 71-74, 86, 90, 93, 105, 114, 131, 132, 138, 144, 147, 154, 155
 

NOAEL . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15, 16, 40, 42, 46, 49, 50, 99, 103, 162
 

NPL . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1, 9, 122-125, 127, 143, 147, 150
 

ocular effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13, 14, 22, 43, 44, 57 
 

organophosphate . . . . . . . . . . . . . . . . . . . . . . . 10-13, 18, 25, 56, 58, 69, 72, 79, 80, 83, 85, 86, 90-92, 94-96, 104, 105, 114, 147,
 

149, 154, 160
 

PAM . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 92, 96 
 

partition coefficients . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112 
 

PBPD . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 74 
 

PBPK . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 74-77 
 

pharmacodynamic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 74 
 

pharmacokinetic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 74-77 
 

photolysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8, 122, 127, 130-133
 

pralidoxime . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 96 
 

pseudocholinesterase . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79, 91 
 

public health . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1, 3, 6, 8, 16, 17, 81, 97, 144, 152, 159
 

pyridine aldoxime methiodide (see PAM) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 92 
 

RCRA ......................................................................................... 120, 167
 

reference dose (see RfD) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 167 
 

regulations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4, 6, 120, 146, 162-165, 167
 

renal effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21, 22, 43, 55 
 

reportable quantity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 120 
 

reproductive system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 50, 102 
 

Resource Conservation and Recovery Act (see RCRA) ................................................... 120, 167
 

restricted-use pesticide . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 116, 162
 

RfD . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 162, 165, 167
 

salivation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10, 22, 24, 26, 79 
 

sea . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 125 
 

sediment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8, 122, 127, 129, 131, 132, 136
 

shrimp . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 116, 131
 

soil . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2, 3, 5, 6, 8, 9, 120, 122, 124, 127-130, 132, 133, 136, 137, 142, 145-148, 158-160, 167
 

solubility ....................................................................................... 112, 129
 

surface water ............................................................................... 125, 127, 147
 

T3 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 82 
 

T4 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 82 
 

time-weighted average . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 53, 167 
 

total diet studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 139 
 

toxicokinetic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16, 99, 100, 105-107
 

Toxics Release Inventory (see TRI) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 114, 124
 

tremors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3, 10, 50, 104 
 

TRI . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12, 114, 120, 124-127, 145
 
METHYL PARATHION D-3 

APPENDIX D 

TWA . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 163, 167
 

USDA . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 117, 149
 

vapor phase . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 130 
 

vapor pressure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112, 128
 

volatility . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 128 
 

volatilization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8, 122, 124, 127, 128