Save the Water™ STEM: Senior water science – water education resources

An Infographic by Open Colleges

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Adopt Your Watershed – This program challenges you to serve your community by taking part in activities to protect and restore your local watershed.

After the Storm – Weather – Weather emergencies such as flooding can introduce pollutants to your water supply. Learn how to protect your source of water and find out what to do in the event that your drinking water is compromised.

Emergency Preparedness – identify some of the issues you may face preparing for, during and after an event that can directly threaten your health and the health of your family.

Good Samaritan – An Agency-wide initiative to accelerate restoration of watersheds and fisheries threatened by abandoned hard rock mine runoff. The Good Samaritan initiative encourages voluntary cleanups by parties that are not responsible for the property in question.

Nonpoint Source Toolbox - Contains a variety of resources for the development of an effective outreach campaign to educate the public on nonpoint source pollution or storm water runoff.

Pollution Prevention – Water pollution and control measures are critical to improving water quality and lessening the need for costly wastewater and drinking water treatment. Find information on a variety of water pollution prevention and control measures.

Protect Your Health – Offers information on how to protect yourself from water-related health risks such as microbes in tap water and in water bodies used for swimming, and contaminants in fish and shellfish.

Protecting Drinking Water – People who travel abroad know the familiar problem with unsafe drinking water. At home, we scarcely give it a thought. Usually, we are right. But the sources of our drinking water are constantly under siege from naturally occurring events and human activities that can pollute our sources of drinking water.

Volunteer Monitoring

Water Efficiency – Efficient use of water helps reduce the demands on our water supplies, as well as on both drinking water and wastewater infrastructure, as using less water means moving and treating less water.

The following articles are from experts in their field: Click on their links to learn more about formaldehyde:

Formaldehyde CAS No: 50-00-0

Formaldehyde is used primarily to make urea-, phenol- and melamine-formaldehyde resins. Other large applications include polyacetal resins, pentaerythritol, methyl di-p-phenylene isocyanate (MDI), and 1,4-butanediol(BDO). Consumption of formaldehyde depends mainly on the construction, automotive and furniture markets. In the developed world, growth in demand will typically track gross domestic product (GDP) although it will be strongly correlated to the construction industry. Prices of formaldehyde are closely tied to and generally track its methanol feedstock. For this reason, ICIS does not publish price reports on formaldehyde.

There are two main processes for making formaldehyde: oxidation-dehydrogenation using a silver catalyst involving either the complete or incomplete conversion of methanol; and the direct oxidation of methanol to formaldehyde using metal oxide catalysts (Formox process).

Formaldehyde is a clear, water-white, very slightly acid, gas or liquid with a strong pungent irritating odour. It is a poison and can be fatal or cause blindness if swallowed. Formaldehyde is a flammable liquid and vapour, and the gas mixes well with air to form explosive mixtures.

Formaldehyde Process Technologies

The commercial production of formaldehyde was first started in Germany in the 1880s but the development of a methanol synthesis route in the 1920s gave the spur to the development of large-scale manufacture. Today there are two main routes: oxidation-dehydrogenation using a silver catalyst involving either the complete or incomplete conversion of methanol; and the direct oxidation of methanol to formaldehyde using metal oxide catalysts (Formox process).
More about Formaldehyde Process Technologies

United States Dept. of Labor

www.OSHA.gov

III. Properties, Manufacture, and Uses of Formaldehyde

The chemical “formaldehyde” is a colorless, pungent gas at room temperature with an approximate odor threshold of about 1 ppm [Ex. 73-120]. While the term “formaldehyde” is also used to describe various mixtures of formaldehyde, water, and alcohol, the term “formalin” more precisely describes aqueous solutions, particularly those containing 37 to 50 percent formaldehyde and 6 to 15 percent alcohol stabilizer. Most formaldehyde enters commerce as formalin. Alcoholic solutions of formaldehyde are available for processes that require low water content [Ex. 73-53]. Paraformaldehyde, a solid, also serves as a source of formaldehyde gas.

Formaldehyde gas per se is not available commercially. The Chemical Abstracts Service (CAS) has assigned the number “50-00-0″ to formaldehyde. This number applies to both formaldehyde gas and its aqueous or alcohol stabilized solutions.

Formaldehyde is a major industrial chemical, ranked 24th in production volume in the United States [Ex. 138-F]. In 1985, 5.7 billion pounds of 37 percent formaldehyde (by weight) was produced. Formaldehyde has four basic uses: as an intermediate in the production of resins; as an intermediate in the production of industrial chemicals; as a bactericide or fungicide; and as a component in the formulation of end-use consumer items. The manufacture of three types of resins: urea-formaldehyde, phenol-formaldehyde, and melamine formaldehyde, accounts for about 59 percent of total consumption [Exs. 70-2; 73-52]. An additional seven percent is consumed in the production of thermoplastic acetal resins [Ex. 8]. About one-third is used in the synthesis of high volume chemical derivatives, including pentaerythritol, hexamethylenetetramine, and butanediol [Ex. 8]. Two percent is used in textile treating and small amounts of formaldehyde are present as preservatives or bactericides in consumer and industrial products, such as cosmetics, shampoos and glues.

Some products prepared from formaldehyde contain unreacted formaldehyde residues which may be released from the product over its useful life. One example is urea-formaldehyde resin. Urea-formaldehyde resin is a generic name that actually represents an entire class of related formulations. Over 60 percent of urea-formaldehyde resin production in 1977 was consumed by particleboard and plywood manufacturing, where the resin is used as a glue. Urea-formaldehyde resins are also used in decorative laminates, textiles, paper, and foundry sand molds [Ex. 73-53].

Formaldehyde resins are used to treat textiles to impart wrinkle-resistance to clothing. About 60-85 percent of all apparel fabric is finished with formaldehyde-containing resins. As apparel manufacture is the sixth largest industry sector in the United States [Exs. 70-2; 70-14], this use is the major source of widespread exposure to formaldehyde because of the large number of workers potentially exposed.

Formaldehyde destroys bacteria, fungi, molds, and yeast. Its commercial importance as a fungicide is probably its greatest use as a disinfectant [Ex. 70-2]. Because of its bactericidal properties, formaldehyde is used in numerous cosmetic preparations.

Formaldehyde’s uses can lead to widespread exposure in downstream industries. For example, when formaldehyde is present in disinfectants, preservatives, and embalming fluid, worker exposure can occur. Although formaldehyde changes into other chemicals when urea-formaldehyde resins and concentrates are produced, decay may occur, causing workers in numerous industries including wood products and apparel manufacture to be exposed to airborne formaldehyde when it offgasses from products manufactured with these resins.

Image: www.thompsonhine.com

GoodGuide

[June 7^th 2012]

Flouride health effects: click>>

HEALTH EFFECTS DATABASE

• Overview Page
• Glossary of Terms
• Bibliography
• Newsletter
• Useful Links

FLUORIDE & DENTAL FLUOROSIS

• Overview Page
• Dental Fluorosis Classification Criteria
• Mild Forms of Dental Fluorosis
• Moderate to Severe Dental Fluorosis
• Perception and Psychological Impact of Dental Fluorosis
• Dental Fluorosis & Elevated Fluoride
• Exposure as a Cause of Tooth Decay
• Biology of Dental Fluorosis

FLUORIDE & TOOTH DECAY

• Overview Page
• “Universal Decline of Tooth Decay” Irrespective of Water Fluoridation
• Topical Vs. Systemic Effects
• Fluoride’s Impact on Smooth Tooth Surfaces vs Pit & Fissures
• Water Fluoridation & Tooth Decay (Caries)
• Fluoridation Cessation Studies
• Water Fluoridation & Poverty

FLUORIDE & the BRAIN

• Overview Page
• Human Studies: Fluoride’s Impact on IQ
• Human Studies: Fluoride’s Impact on the Developing Brain (Fetuses/Infants)
• Human Studies: Fluoride’s Impact on the Adult Brain
• Animal Studies: Fluoride’s Impact on Brain (Behavior/ Learning/ Memory)
• Animal Studies: Fluoride’s Impact on Brain

INFANT FLUORIDE WARNINGS

• Overview Page
• Fluoride Supplementation No Longer Recommend for Newborns
• Recommendations from Dental Researchers
• Breast-fed infants protected from fluoride
• Formula-fed babies receive 100-200 times more fluoride than breast-fed babies
• High Fluoride Exposure During Infancy – A 20th Century Phenomena
• Infants have impaired ability to excrete fluoride
• Formula made with fluoridated water a risk factor for dental fluorosis
• Is dental fluorosis just a ‘cosmetic effect’?

FLUORIDE & ARTHRITIS Overview Page

• Fluoride & Osteoarthritis
• Fluoride & Rheumatoid Arthritis
• Fluoride & DISH (Diffuse Idiopathic Skeletal Hyperostosis)
• Fluoride & Spondylosis/Spondylitis

FLUORIDE & BONE

A) Fluoride & Bone Fracture:

• Overview Page
• Fluoride & Bone Strength
• Epidemiology on Fluoride & Bone Fracture
• Fluoride-Induced Bone Fractures in Human Clinical Trials
• Mechanisms by which fluoride may reduce bone strength

B) Fluoride & Bone Density:

• Overview Page
• Fluoride’s Differential Effect on Bone Density
• Fluoride-induced Increase in Bone Density: Not associated with Increased Strength
• Fluoride & Bone Density: Epidemiology

C) Skeletal Fluorosis:

• Overview Page
• The Difficulty of Diagnosis
• “Pre-skeletal” Fluorosis
• X-Ray Diagnosis of Skeletal Fluorosis
• Skeletal Fluorosis in the U.S.
• Skeletal Fluorosis in India & its Relevance to the West
• High Individual Variability in Skeletal Response to Fluoride
• Factors which may increase susceptibility to fluorosis
• Variability in Radiographic Appearance of Fluorosis
• Variable Length of Exposure Producing Fluorosis
• Estimated “Threshold” Doses for Skeletal Fluorosis
• Water Fluoride Levels Associated with Skeletal Fluorosis
• Fluoridation, Dialysis, & Osteomalacia
• Fluoride & Renal Osteodystrophy
• Fluoride & Osteomalacia
• Fluoride & Rickets
• Fluoride & Osteoid
• Fluoride & Secondary Hyperparathyroidism
• Fluoride & Osteopetrosis
• Fluoride & Spinal Cord Compression
• Crippling Skeletal Fluorosis

FLUORIDE & CANCER

• Overview Page
• Fluoride & Mutagenicity
• Fluoride & Osteosarcoma
• Fluoride & Osteosarcoma Timeline
• NTP Bioassay on Fluoride/Cancer (1990)
• Fluoride & Liver Tumors in NTP Fluoride/Cancer Study
• Interview with Dr. William Marcus (EPA)
• Dr. William Marcus’ Internal Memo
• Interview with Dr. William Hirzy (EPA)

[May 19^th 2012]

Flouride health effects data base cont’d: click>>

FLUORIDE HEALTH EFFECTS DATABASE

FLUORIDE & the BRAIN (Click for more detail)

Fluoride’s ability to damage the brain represents one of the most active areas of research on fluoride toxicity today.

Concern about fluoride’s impact on the brain has been fueled by 18 human studies (from China, Mexico, India, and Iran) reporting IQ deficits among children exposed to excess fluoride, by 4 human studies indicating that fluoride can enter, and damage, the fetal brain; and by a growing number of animal studies finding damage to brain tissue (at levels as low as 1 ppm) and impairment of learning and memory among fluoride-treated groups.

According to the US National Research Council, “it is apparent that fluorides have the ability to interfere with the functions of the brain.”

FLUORIDE
& the PINEAL GLAND (Click for more detail)

Summation – Fluoride & Pineal Gland:

Up until the 1990s, no research had ever been conducted to determine the impact of fluoride on the pineal gland – a small gland located between the two hemispheres of the brain that regulates the production of the hormone melatonin. Melatonin is a hormone that helps regulate the onset of puberty and helps protect the body from cell damage caused by free radicals.

It is now known – thanks to the meticulous research of Dr. Jennifer Luke from the University of Surrey in England – that the pineal gland is the primary target of fluoride accumulation within the body.

READ MORE AT FLUROIDEALERT.org

FLUORIDE & BONE DISEASE (Click for more detail)

Excessive exposure to fluoride is well known to cause a bone disease called skeletal fluorosis.

Skeletal fluorosis, especially in its early stages, is a difficult disease to diagnose, and can be readily confused with various forms of arthritis including osteoarthritis and rheumatoid arthritis.

In its advanced stages, fluorosis can resemble a multitude of bone/joint diseases.

In individuals with kidney disease, fluoride exposure can contribute to, and/or exacerbate, renal osteodystrophy.

READ MORE AT FLUORIDEALERT.ORG

FLUORIDE & the KIDNEYS (Click for more detail)

The kidneys play a vital role in preventing the build-up of excessive fluoride in the body. Among healthy individuals, the kidneys excrete approximately 50% of the daily fluoride intake. However, among individuals with kidney disease, the kidneys’ ability to excrete becomes markedly impaired, resulting in a build-up of fluoride within the body.

It is well recognized that individuals with kidney disease have a heightened susceptibility to the cumulative toxic effects of fluoride.

Of particular concern is the potential for fluoride, when accumulated in the skeletal system, to cause, or exacerbate, renal osteodystrophy – a bone disease commonly found among people with advanced kidney disease.

READ MORE AT FLUORIDEALERT.ORG

January 2010; Updated March 30, 2012

• Overview
• Background
• FDA’s Current Perspective on BPA
• Additional Studies
• Public Comment and Next Steps for FDA’s Assessment of BPA
• Interim Public Health Recommendations
• The Regulatory Framework for BPA
• Collaboration with International Partners
• Original January 2010 update available in PDF (52KB).

Overview

Bisphenol A (BPA) is an industrial chemical that has been present in many hard plastic bottles and metal-based food and beverage cans since the 1960s.

Studies employing standardized toxicity tests have thus far supported the safety of current low levels of human exposure to BPA. However, on the basis of results from recent studies using novel approaches to test for subtle effects, both the National Toxicology Program at the National Institutes of Health and FDA have some concern about the potential effects of BPA on the brain, behavior, and prostate gland in fetuses, infants, and young children. In cooperation with the National Toxicology Program, FDA’s National Center for Toxicological Research is carrying out in-depth studies to answer key questions and clarify uncertainties about the risks of BPA.

In the interim:

• FDA is taking reasonable steps to reduce human exposure to BPA in the food supply. These steps include:
  • supporting the industry’s actions to stop producing BPA-containing baby bottles and infant feeding cups for the U.S. market;
  • facilitating the development of alternatives to BPA for the linings of infant formula cans; and
  • supporting efforts to replace BPA or minimize BPA levels in other food can linings.
• FDA is supporting a shift to a more robust regulatory framework for oversight of BPA.
• FDA is seeking further public comment and external input on the science surrounding BPA.

FDA is also supporting recommendations from the Department of Health and Human Services for infant feeding and food preparation to reduce exposure to BPA.

FDA is not recommending that families change the use of infant formula or foods, as the benefit of a stable source of good nutrition outweighs the potential risk from BPA exposure.

Background

BPA is an industrial chemical used to make a hard, clear plastic known as polycarbonate, which has been used in many consumer products, including reusable water bottles. BPA is also found in epoxy resins, which act as a protective lining on the inside of metal-based food and beverage cans. These uses of BPA are subject to premarket approval by FDA as indirect food additives or food contact substances. The original approvals were issued under FDA’s food additive regulations and date from the 1960s.

Studies employing standardized toxicity tests used globally for regulatory decision making thus far have supported the safety of current low levels of human exposure to BPA.[1] However, results of recent studies using novel approaches and different endpoints describe BPA effects in laboratory animals at very low doses corresponding to some estimated human exposures.[2] Many of these new studies evaluated developmental or behavioral effects that are not typically assessed in standardized tests.

The National Toxicology Program Center for the Evaluation of Risks to Human Reproduction, part of the National Institutes of Health, completed a review of BPA in September 2008.[3] The National Toxicology Program uses five different terms to describe its level of concern about the different effects of chemicals: negligible concern, minimal concern, some concern, concern, and serious concern.[4]

In its report on BPA, the National Toxicology Program expressed “some concern for effects on the brain, behavior, and prostate gland in fetuses, infants, and children at current human exposures to bisphenol A.”[5] The Program also expressed “minimal concern for effects on the mammary gland and an earlier age for puberty for females in fetuses, infants, and children at current human exposures to bisphenol A” and “negligible concern” for other outcomes.[6]

The National Toxicology Program does not make regulatory recommendations. With respect to neurological and developmental outcomes of BPA, the Program stated that “additional research is needed to more fully assess the functional, long-term impacts of exposures to bisphenol A on the developing brain and behavior.”[7] The Program also stated:

Overall, the current literature cannot yet be fully interpreted for biological or experimental consistency or for relevance to human health. Part of the difficulty for evaluating consistency lies in reconciling findings of different studies that use different experimental designs and different specific behavioral tests to measure the same dimension of behavior.[8]

In August 2008, prior to the release of the final National Toxicology Program report, FDA released a document entitled Draft Assessment of Bisphenol A for Use in Food Contact Applications.[9] This draft assessment was then reviewed by a Subcommittee of FDA’s Science Board, which released its report at the end of October 2008.[10]

Since that time, the Center for Food Safety and Applied Nutrition (CFSAN) within FDA has reviewed additional studies of low-dose toxicity cited by the National Toxicology Program and the Science Board Subcommittee as well as other such studies that have become available. The Center then prepared a document entitled Bisphenol A (CAS RN. 80-05): Review of Low Dose Studies,dated August 31, 2009. In the fall of 2009, FDA’s Acting Chief Scientist asked five expert scientists from across the federal government to provide independent scientific evaluations of this document. In April 2010, FDA made the CFSAN documents available for public comment, and also made public the independent scientific evaluations.

FDA is continuing to consider the low dose toxicity studies of BPA as well as other recent peer-reviewed studies related to BPA. At this stage, FDA is explaining its current perspective on BPA, its support for further studies, its establishment of a public docket for its assessment of BPA use in food contact applications, its interim public health recommendations, its view of the appropriate regulatory framework for BPA use in food contact applications, and our collaborations with international partners.

FDA’s Current Perspective on BPA

At this interim stage, FDA shares the perspective of the National Toxicology Program that recent studies provide reason for some concern about the potential effects of BPA on the brain, behavior, and prostate gland of fetuses, infants and children. FDA also recognizes substantial uncertainties with respect to the overall interpretation of these studies and their potential implications for human health effects of BPA exposure. These uncertainties relate to issues such as the routes of exposure employed, the lack of consistency among some of the measured endpoints or results between studies, the relevance of some animal models to human health, differences in the metabolism (and detoxification) of and responses to BPA both at different ages and in different species, and limited or absent dose response information for some studies.

FDA is pursuing additional studies to address the uncertainties in the findings, seeking public input and input from other expert agencies, and supporting a shift to a more robust regulatory framework for oversight of BPA to be able to respond quickly, if necessary, to protect the public.

In addition, FDA is supporting reasonable steps to reduce human exposure to BPA, including actions by industry and recommendations to consumers on food preparation. At this time, FDA is not recommending that families change the use of infant formula or foods, as the benefit of a stable source of good nutrition outweighs the potential risk of BPA exposure.

Additional Studies

FDA supports additional studies, by both governmental and non-governmental entities, to provide additional information and address uncertainties about the safety of BPA.

FDA’s Studies. FDA’s CFSAN and FDA’s National Center for Toxicological Research has been and continues to pursue a set of studies on the exposure to dietary BPA and the safety of low doses of BPA, including assessment of the novel endpoints where concerns have been raised. These include studies pursued in collaboration with the National Toxicology Program and with support and input from the National Institute for Environmental Health Sciences.

Recent evaluation by the FDA’s CFSAN has:

• Determined that exposure to dietary BPA for infants, the population of most potential concern, is less than previously estimated. The initial FDA exposure estimates were 0.185 micrograms/kg-bw/day for adults and 2.42 micrograms/kg bw/day for infants. The new estimate of average dietary exposure, based on increased data collection, is 0.2-0.4 micrograms/kw-bw/day for infants and 0.1-0.2 micrograms/kg-bw/day for children and adults.

Recent research studies pursued by FDA’s National Center for Toxicological Research have[11-17]:

• Found evidence in rodent studies that the level of the active form of BPA passed from expectant mothers to their unborn offspring, following oral exposure, is so low it could not be measured. The study orally dosed pregnant rodents with 100-1000 times more BPA than people are exposed to through food, and could not detect the active form of BPA in the fetus 8 hours after the mother’s exposure.
• Demonstrated that oral BPA administration results in rapid metabolism of BPA to an inactive form. This results in much lower internal exposure of aglycone BPA (i.e., the active form) than what occurs from other routes of exposure such as injection. Primates of all ages were also found to effectively metabolize BPA to its inactive form and excrete it much more rapidly and efficiently than rodents, thus reducing concerns about results from some rodent studies using oral and, particularly, non-oral exposures which result in higher actual internal exposures of rodents than of primates, including humans, exposed to the same dose.
• Developed a physiologically based pharmacokinetic model which can be used to predict the level of internal exposure to the active and inactive forms of BPA. This model allows comparisons of internal exposure across different ages and routes of exposure (e.g., oral and intravenous routes). Based on the effects of metabolism, internal exposures to aglycone BPA following oral administration are predicted to be below 1% or less of the total BPA level administered.

The FDA’s National Center for Toxicological Research is continuing with additional studies, including:

• Rodent subchronic studies which are in progress to characterize potential effects, and, where observed, the dose-response relationship in the prostate and mammary glands for orally administered BPA. In addition, these studies will explore other issues including potential effects of BPA on metabolic changes and cardiovascular endpoints. These studies will include an in utero phase, mimic bottle feeding in neonates, and employ a dose range that will cover the low doses where effects have been previously reported in some animal studies, as well as higher doses where estrogenic effects have been measured in guideline oral studies. Results from this study are expected to be available to FDA to inform the agency’s decision making starting in 2012.

• Rodent behavioral/neuroanatomical pilot studies which are also already in progress as part of the sub-chronic study to characterize dose levels at which behavioral, neuroanatomical, neurochemical and hormonal endpoints may be affected by developmental exposure to BPA. These data are intended to evaluate possible effects of exposure to BPA during development that have been reported in some published studies on sexually dimorphic behavioral endpoints such as anxiety, as well as on standard developmental neurotoxicity tests. Results from these studies are expected to be available to FDA to inform the agency’s decision making starting in 2012.

Other Studies. Other studies on the safety of BPA are also underway. For example, the National Toxicology Program/Food and Drug Administration (NTP/FDA) will conduct a long-term toxicity study of BPA in rodents to assess a variety of endpoints including novel endpoints where concerns have been raised. NTP/FDA will collaborate with the National Institute of Environmental Health Sciences by providing animals and tissues to a consortium of researchers with interest in studying a variety of additional toxicological areas.

Public Comment and Next Steps for FDA’s Assessment of BPA

On April 5, 2010 the FDA opened a public docket (FDA-2010-N-0100) for comment on BPA. The docket contains the Center for Food Safety and Applied Nutrition’s review of the low dose toxicity studies and recently published studies, the five expert reviews, other relevant material, and public comments.

FDA will also continue to consult with other expert agencies in the federal government, including the National Institutes of Health (and National Toxicology Program), Environmental Protection Agency, Consumer Product Safety Commission, and the Centers for Disease Control and Prevention.

Based on this outside input and the results of new studies, FDA will update its assessment of BPA and will be prepared to take additional action if warranted. As the scientific field is evolving rapidly, FDA anticipates providing further updates on BPA to the public as significant new information becomes available.

Interim Public Health Recommendations

At this interim stage, FDA supports reasonable steps to reduce exposure of infants to BPA in the food supply. In addition, FDA will work with industry to support and evaluate manufacturing practices and alternative substances that could reduce exposure to other populations.

Infants. Infants are a potentially sensitive population for BPA because (1) their neurological and endocrine systems are developing; and (2) their hepatic system for detoxification and elimination of such substances as BPA may be immature.

• FDA is supporting the industry’s actions to stop producing BPA-containing bottles and infant feeding cups for the U.S. market. FDA understands that the major manufacturers of these products have stopped selling new BPA-containing bottles and infant feeding cups for the U.S. market. Glass and polypropylene bottles and plastic disposable “bag” liners have long been alternatives to polycarbonate nursing bottles.

• FDA is facilitating the development of alternatives to BPA for the linings of infant formula cans. FDA has already noted increased interest on the part of infant formula manufacturers to explore alternatives to BPA-containing can linings, and has received notifications for alternative packaging. The agency is supporting efforts to develop and use alternatives by (1) working with manufacturers regarding the regulatory status and safety of alternative liners; (2) giving technical assistance to those wishing to prepare applications for approval of alternatives; and (3) expeditiously reviewing any such new applications for alternatives. Because reliable can lining materials are a critical factor in ensuring the quality of heat processed liquid infant formula, safe replacement of such materials requires not only that they both be safe for food contact but also allow for processing that is fully functional in protecting the safety and quality of the infant formula itself.

The American Academy of Pediatrics and other health authorities recommend breastfeeding as the optimal nutrition for infants. Infant formula, including infant formula packaged in cans, is a safe and acceptable alternative that provides known nutritional benefits and prevents life-threatening nutritional deficiencies.

FDA is not recommending that families change the use of infant formula or foods, as the benefit of a stable source of good nutrition outweighs the potential risk of BPA exposure.

Other Advice. FDA is supporting recommendations by the Department of Health and Human Services for infant feeding and food preparation to reduce exposure to BPA.

The Regulatory Framework for BPA

Current BPA food contact uses were approved under food additive regulations issued more than 40 years ago. This regulatory structure limits the oversight and flexibility of FDA. Once a food additive is approved, any manufacturer of food or food packaging may use the food additive in accordance with the regulation. There is no requirement to notify FDA of that use. For example, today there exist hundreds of different formulations for BPA-containing epoxy linings, which have varying characteristics. As currently regulated, manufacturers are not required to disclose to FDA the existence or nature of these formulations. Furthermore, if FDA were to decide to revoke one or more approved uses, FDA would need to undertake what could be a lengthy process of rulemaking to accomplish this goal.

Since 2000, FDA has regulated new food contact substances through the Food Contact Notification Program. Under this program:

• FDA receives notification from each manufacturer of the basis for the safe use of a food contact substance, detailing the conditions of the substance’s use, allowing the agency and public to know how much is being used, and for what applications;
• FDA can work with individual manufacturers to minimize exposure if a potential or actual safety concern is identified after approval;
• FDA can require the submission of additional safety and exposure data from individual manufacturers to address a significant safety concern;
• FDA can require additional studies by individual manufacturers to address a significant safety concern; and
• If FDA were to reach a conclusion that revocation of one or more approved uses is justified, FDA could quickly protect the public by revoking the use through a notice published in the Federal Register.

Given concern about BPA, and the ongoing evaluation of and studies on its safety, FDA believes that the more modern framework is more robust and appropriate for oversight of BPA than the current one.

FDA will encourage manufacturers to voluntarily submit a food contact notification for their currently marketed uses of BPA-containing materials.

In addition, FDA will explore additional options to regulate BPA under the more modern framework.

Collaboration with International Partners

FDA will continue to participate in discussions with our international regulatory and public health counterparts who have also been engaged in assessing the safety of BPA.

For example, FDA has participated with Health Canada in encouraging industry efforts to refine their manufacturing methods for the production of infant formula can linings to minimize migration of BPA into the formula.

In addition, FDA actively supported and participated in the Expert Consultation on BPA convened by World Health Organization and the Food and Agriculture Organization of the United Nations on November 2-5, 2010, in Ottawa, Canada. Information about this expert consultation and the report of the meeting is available from the WHO web site .

Back to Top

[1]See, e.g., European Food Safety Authority. Toxicokinetics of Bisphenol A, Scientific Opinion of the Panel on Food additives, Flavourings, Processing aids and Materials in Contact with Food, Adopted 9 July 2008 , The EFSA Journal 2008.

[2]See, e.g. vom Saal FS, Akingbemi BT, Belcher SM et al. Chapel Hill bisphenol A expert panel consensus statement: integration of mechanisms, effects in animals and potential to impact human health at current levels of exposure, Reproductive Toxicology 2007;24:131-8.

[3]NTP-CERHR Monograph on the Potential Human Reproductive and Developmental Effects of Bisphenol A, NIH Publication No. 08-5994, September 2008.

[4]Ibid, page 6.

[5]Ibid.

[6]Ibid.

[7]Ibid, page 20.

[8]Ibid.

[9]U.S. Food and Drug Administration, Draft Assessment of Bisphenol A for Use in Food Contact Applications, 14 August 2008.

[10]FDA Science Board Subcommittee on Bisphenol A. Scientific Peer-Review of the Draft Assessment of Bisphenol A for Use in Food Contact Applications, 31 October 2008.

[11]Doerge D.R., Twaddle N.C., Woodling K.A., Fisher J.W. Pharmacokinetics of bisphenol A in neonatal and adult rhesus monkeys, Toxicology and Applied Pharmacology 2010; 248: 1–11.

[12]Doerge D.R., Twaddle N.C., Vanlandingham M., Fisher J.W. Pharmacokinetics of Bisphenol A in neonatal and adult CD-1 mice: Inter-species comparisons with Sprague-Dawley rats and rhesus monkeys, Toxicology Letters 2011; 207: 298– 305.

[13]Doerge D.R., Twaddle N.C., Vanlandingham M., Brown R.P., Fisher J.W. Distribution of bisphenol A into tissues of adult, neonatal, and fetal Sprague–Dawley rats, Toxicology and Applied Pharmacology 2011; 255: 261–270.

[14]Doerge D.R., Vanlandingham M., Twaddle N.C., Delclos K.B. Lactational transfer of bisphenol A in Sprague–Dawley rats, Toxicology Letters 2010; 199: 372–376.

[15]Twaddle N.C., Churchwell M.I., Vanlandingham M., Doerge D.R. Quantification of deuterated bisphenol A in serum, tissues, and excreta from adult Sprague Dawley rats using liquid chromatography with tandem mass spectrometry, Rapid Communications in Mass Spectrometry 2010; 24: 3011–3020.

[16]Doerge D.R., Twaddle N.C., Vanlandingham M., Fisher J.W. Pharmacokinetics of bisphenol A in neonatal and adult Sprague-Dawley rats, Toxicology and Applied Pharmacology 2010; 247: 158–165.

[17]Fisher J.W., Twaddle N.C., Vanlandingham M., Doerge D.R. Pharmacokinetic Modeling: Prediction and Evaluation of Route Dependent Dosimetry of Bisphenol A in Monkeys with Extrapolation to Humans, Toxicology and Applied Pharmacology 2011; 257; 122-136.

6 Health Dangers of BPA

January 25, 2010

Bisphenol-A, or BPA, is an industrial chemical used in plastics and canned food linings. It is an organic compound that acts similarly to estrogen when ingested into the body. A growing number of health experts and consumers are becoming concerned about the adverse health effects that can be caused from high-dose or long-term exposure to BPA.

1. Heart Disease

The most recent study regarding BPA has shown a confirmed link to heart disease. Researchers from England reviewed data from the National Health and Nutrition Examination Surveys and found that men with the highest levels of BPA exposure, as determined from urinary samples, were 10% more likely to develop heart disease. BPA is thought to suppress a hormone that protects people from having heart attacks, oxidative stress, and damages to the endothelial cells of blood vessels.

2. Intestinal Damage

French researchers published data recently that links BPA with the functioning ability of the intestines, as this is the first organ to come in contact with the chemical after it is ingested from food and beverage containers. The study was conducted on animals, using a level that was 10 times below a level currently thought to be safe for humans. The mucosal lining of the intestinal wall failed, causing a condition called “leaky gut syndrome.” Damage to the lining can cause failure of the blockage of toxins and bacteria, which can then enter the body and cause damage to tissues and organs.

3. Infertility and Reproductive Issues

Another animal study found that chronic exposure to even low-doses of BPA can impair the growth and function of female antral follicles, the egg cell which is involved in ovulation. Because the chemical structure of BPA is similar to estrogen, it binds with receptors in the cells, causing a decrease in other important female hormones, such as progesterone.

4. Erectile Dysfunction

Another recent study focused on the hormonal effect on men. The journal Human Reproduction published research on over 200 Chinese men who were exposed to BPA in their workplace. Those men were four times more likely to have erectile dysfunction and seven times more likely to have ejaculation difficulties. The level of chemical exposure in the study was more than 50 times a level that the average American would be exposed to, but the study points out the effect that a hormonal compound can have on the male reproductive system in high doses.

5. Diabetes and Obesity

BPA is also linked to diabetes and metabolic syndrome, two conditions caused by a decrease in the body’s ability to effectively use insulin. BPA causes an increase in insulin output from the beta cells of the pancreas. High levels of circulating insulin causes a reduction in the body’s ability to break down fat, which leads to a greater risk of obesity.

6. Behavioral Changes in Children

A study from the University of Chapel Hill highlighted the dangers of children exposed to BPA from baby bottles and baby food containers. Toddler girls exposed to BPA were considered more aggressive and hyperactive than those with less exposure. Other research in children has shown that BPA is present in the umbilical cords of newborns, suggesting that the mother’s exposure can affect her offspring.

The Future of BPA

The US. Food and Drug Administration is reviewing the data on BPA and is expected to release an assessment in the coming months. Until then, the National Institute of Environmental Health Sciences (NIEHS) is recommending that consumers reduce their current exposure levels by decreasing the use of certain plastic containers that use BPA and opt for glass, porcelain or stainless steel instead.

Related posts:

• 8 Hidden Sources of BPA
• How a Carcinogen Harms Your Health
• Obese? Why BPA in Food May Be to Blame

ATSDR: Camp Lejeune, and tetrachloroethylene (PCE)

Camp Lejeune, North Carolina

Agency for Toxic Substances and Disease Registry, 4770 Buford Hwy NE, Atlanta, GA 30341 / Contact CDC: 800-232-4636 / TTY: 888-232-6348

Reported health effects linked with trichloroethylene (TCE), tetrachloroethylene (PCE), benzene, and vinyl chloride (VC) exposure

Reported health effects linked with TCE, PCE, benzene, and VC exposure in people

Q: What did the 1998 ATSDR health study “Volatile Organic Compounds in Drinking Water and Adverse Pregnancy Outcomes” at Camp Lejeune find?

A: Overall, the study found a link between PCE-contaminated drinking water and lower birth weights for infants of older mothers and mothers with histories of fetal loss. PCE-contaminated drinking water was also linked with small-for-gestational-age infants for older mothers and mothers with two or more prior fetal losses. This study could not look at fetal deaths because existing records were not complete. Because of errors in the exposure information available at that time, ATSDR will reanalyze this study when the water modeling is completed.

Q: What have other studies found about the persistent health effects of TCE, PCE, benzene, and VC?

A: The effects of exposure to any chemical depend on—

• When you are exposed (during pregnancy, in infancy),
• How much you are exposed to,
• How long you are exposed,
• How you are exposed (breathing, drinking), and
• What your personal traits and habits are.

Therefore, not everyone who is exposed to TCE, PCE, benzene, or VC will develop a health problem.

A limited number of studies have been done that looked at the health problems in children and adults related to drinking water contaminated with TCE and PCE. Only one study (in New Jersey) has looked at the health problems in children related to drinking water contaminated with benzene or VC. However, too few children were exposed to benzene or VC in that study to reach any conclusion about health problems. No studies have looked at the health problems in adults related to drinking water contaminated with benzene and VC.

A much larger number of studies have looked at health problems among workers exposed to TCE, PCE, benzene, and VC. Below is a list of the types of health outcomes that have been found to be linked to TCE, PCE, benzene, and VC. The numbers in parentheses indicate the reference for the study. All of the references are listed at the end.

Reported health problems in children who were exposed in the womb from their mother drinking water contaminated with TCE and/or PCE include—

• Leukemia (1-3)
• Small for gestational age (4-6)
• Low birth weight (6-8)
• Fetal death (4, 7, 9)
• Major heart defects (7, 10)
• Neural tube defects (4, 7, 9)
• Oral cleft defects (including cleft lip) (4, 7, 9)
• Chonal atresia (nasal passages blocked with bone or tissue) (4, 9)
• Eye defects (4, 9)

Reported health problems in children who were exposed in the womb from their mother working with TCE and/or PCE include—

• Low birth weight (11)
• Miscarriage (12, 13)
• Major malformations (11)

Reported health problems in people of all ages from drinking water contaminated with TCE and/or PCE include—

• Non-Hodgkins lymphoma (1, 12)
• Leukemia (1, 17)
• Rectal cancer (14)
• Bladder cancer (17)
• Breast cancer (18)
• Lung cancer (14)

Reported health problems in people of all ages from working with TCE and/or PCE include—

• Hodgkins disease (15)
• Non-Hodgkins lymphoma (15)
• Cervical cancer (15)
• Esophageal cancer (15, 30, 31)
• Kidney cancer (15)
• Liver/biliary cancer (15)
• Ovarian cancer (15)
• Prostate cancer (15)
• End-stage renal disease (29)
• Neurological effects (delayed reaction times problems with short-term memory, visual perception, attention, and color vision) (13)
• Severe, generalized hypersensitivity skin disorder (an autoimmune-related disease) (32)
• Scleroderma (32)

Reported health problems in people of all ages from working with benzene include—

• Non-Hodgkin’s lymphoma (19, 20)
• Leukemias (21, 22)
• Multiple myeloma (23)
• Aplastic anemia (24)
• Miscarriage (24)

Reported health problems in people of all ages from working with VC include—

• Liver cancer (25, 26)
• Soft tissue sarcoma (26)
• Brain cancer (26)
• Lung cancer (27)
• Liver cirrhosis (28)

Workers are exposed to much higher levels of TCE, PCE, benzene, and VC than are people who drink contaminated water. Therefore, the health problems seen in people who worked with TCE, PCE, benzene, and VC may not be seen in people who drank contaminated water.

For health problems not listed in the tables—

• Studies, so far, do not support a link with the particular health outcome and TCE, PCE, benzene, or VC exposure, or
• There is not enough information to see if the outcome is linked to TCE, PCE, benzene, or VC exposure.

Q: How are studies in animals and people different?

A: In studies done in laboratory animals, such as mice, the animals are exposed to much higher levels of chemicals than are people. Animals are also exposed in different ways than are people. In animal studies, we know the exact types and levels of chemicals the animals are exposed to. We can’t tell for certain the exact levels people are exposed to. Also, people are usually exposed to multiple chemicals. Medications, alcohol intake, and lifestyle factors also play a role in how these chemicals affect people.

Reported health effects linked with TCE, PCE, benzene, and VC exposure in animals

Q: What health effects are seen in animal studies of PCE exposure?

A: Results of animal studies showed that PCE can cause liver and kidney damage. The studies also showed that PCE can cause liver cancer in animals. Exposure at very high levels of PCE can be harmful to the unborn pups of pregnant rats and mice. Changes in behavior were seen in the offspring of rats that breathed high levels of the chemical while they were pregnant. Behavioral changes included being hyperactive. Various neurological problems were seen in both the mother and offspring. Neurological problems included being unable to coordinate muscles and decreased movement.

Q: What health effects are seen in animals from TCE exposure?

A: Results of animal studies showed that TCE may cause liver, kidney, or lung cancer. The studies also showed that TCE can cause neurological problems and liver and kidney damage in animals. Neurological problems included being unable to coordinate muscles and decreased movement.

Q: What health effects are seen in animals from benzene exposure?

A: Results of animal studies showed that benzene may cause Zymbal-gland (ear canal) carcinoma, oral-cavity tumors, skin cancer, lymphoma, lung tumors, ovarian tumors, and mammary-gland carcinoma.

Q: What health effects are seen in animals from VC exposure?

A: Results of animal studies showed that VC may cause tumors in the liver, lung,
mammary-gland, Zymbal-gland (ear canal), kidney, skin, and stomach, and angiosarcoma (blood-vessel tumors) and adenocarcinoma (tumors of the linings of organs) at various sites. VC also caused genetic damage including mutations, DNA damage, chromosome damage or loss, chromosomal aberrations (changes in chromosome structure or number), and sister chromatid exchange.

Reported health effects linked with TCE, PCE, benzene, and VC exposure in both people and animals

Q: What health effects are seen in both people and animals from TCE, PCE, benzene, and VC exposure?

A: When there are studies in people, results of animal studies are used to help support any observed links. Results of animal studies are used when there are no studies in people. Reported health effects seen in both people and animals include—

• Lung cancer
• Kidney cancer
• Liver cancer
• Lymphoma
• Breast cancer
• Neurological effects

Some health effects seen in people cannot be tested for in animals.

References

1. Cohn P, Klotz J, Bove F, Fagliano J. 1994. Drinking water contamination and the incidence of leukemia and non-Hodgkin’s lymphoma. Environ Health Perspect 102:556-61.

2. Costas K, Knorr RS, Condon SK. 2002. A case-control study of childhood leukemia in Woburn, Massachusetts: the relationship between leukemia incidence and exposure to public drinking water. Sci Total Environ 300:23-35.

3. New Jersey Department of Health and Senior Services. 2003. Case-control study of childhood cancers in Dover Township (Ocean Country), New Jersey. Trenton, New Jersey: New Jersey Department of Health and Senior Services.

4. Massachusetts Department of Public Health, Centers for Disease Control and Prevention, Massachusetts Health Research Institute. 1996. Final report of the Woburn environmental and birth study. Boston, Massachusetts: Massachusetts Department of Public Health.

5. Agency for Toxic Substances and Disease Registry. 1998. Volatile organic compounds in drinking water and adverse pregnancy outcomes: U.S. Marine Corps Camp Lejeune, North Carolina. Atlanta: US Department of Health and Human Services.

6. Sonnenfeld N, Hertz-Picciotto I, Kaye WE. 2001. Tetrachloroethylene in drinking water and birth outcomes at the US Marine Corps Base at Camp Lejeune, North Carolina. Am J Epidemiol 154(10):902-8.

7. Bove FJ, Fulcomer MC, Klotz JB, Esmart J, et al. 1995. Public drinking water contamination and birth outcomes. Am J Epidemiol 141:850-62.

8. Rodenbeck SE, Sanderson LM, Rene A. 2000. Maternal exposure to trichloroethylene in drinking water and birthweight outcomes. Arch Environ Health 55:188–194.

9. Bove F, Shim Y, Zeitz P. 2002. Drinking water contaminants and adverse pregnancy outcomes: a Review. Environ Health Perspect 110(S): 61-73.

10. Goldberg SJ, Lebowitz MD, Graver EJ, Hicks S. 1990. An association of human congenital cardiac malformations and drinking water contaminants. J Am Coll Cardiol 16:155–164.

11. Khattak S, K-Moghtader G, McMartin K, Barrera M, et al. 1999. Pregnancy outcome following gestational exposure to organic solvents: a prospective controlled study. JAMA 281(12): 1106-09.

12. Pesticide and Environmental Toxicology Section, Office of Environmental Health Hazard Assessment, California Environmental Protection Agency. 1999. Public health goal for trichloroethylene in drinking water. Sacramento, California.

13. Pesticide and Environmental Toxicology Section, Office of Environmental Health Hazard Assessment, California Environmental Protection Agency. 2001. Public health goal for tetrachloroethylene in drinking water. Sacramento, California.

14. Paulu C, Aschengrau A, Ozonoff D. 1999. Tetrachloroethylene-contaminated drinking water in Massachusetts and the risk of colon-rectum, lung, and other cancers. Environ Health Perspect 107(4):265-71.

15. Wartenberg D, Reyner D, Scott CS. 2000. Trichloroethylene and cancer: epidemiologic evidence. Environ Health Perspect 108(S2):161-176.

16. Morgan RW, Kelsh MA, Zhao K, Heringer S. 1998. Mortality of aerospace workers exposed to trichloroethylene. Epidemiology 9(4):424-31.

17. Aschengrau A, Ozonoff D, Paulu C, Coogan P, Vezina R, Heeren T, Zhang Y. 1993. Cancer risk and tetrachloroethylene-contaminated drinking water in Massachusetts. Arch Environ Health. 48:284-92.

18. Aschengrau A, Rogers S, Ozonoff D. 2003. Perchloroethylene-contaminated drinking water and the risk of breast cancer: additional results from Cape Cod, Massachusetts, USA. Environ Health Perspect 111(2):167-73.

19. Steinmaus C, Smith AH, Jones RM, Smith MT. 2008. Meta-analysis of benzene exposure and non-Hodgkin’s lymphoma: Biases could mask an important association. Occup. Environ. Med. 65(6):371-8.

20. Mehlman MA. 2006. Causal relationship between non-Hodgkin’s lymphoma and exposure to benzene and benzene-containing solvents. Ann. N.Y. Acad. Sci. 1076:120–128.

21. Rinsky RA, Hornung RW, Silver SR, Tseng CY. 2002. Benzene exposure and hematopoietic mortality: A long-term epidemiologic risk assessment. Am J Ind Med. 42(6):474-80

22. Glass DC, Gray CN, Jolley DJ, Gibbons C, et al. 2003. Leukemia risk associated with low-level benzene exposure. Epidemiology. 14(5):569-577.

23. Infante PF. 2006. Benzene Exposure and Multiple Myeloma: A Detailed Meta-analysis of Benzene Cohort Studies. Ann. N.Y. Acad. Sci. 1076:90–109.

24. Khan HA. 2007. Short Review: Benzene’s toxicity: a consolidated short review of human and animal studies. Hum Exp Toxicol. 26; 677-685.

25. Bosetti C, La Vecchia C, Lipworth L, McLaughlin JK. 2003. Occupational exposure to vinyl chloride and cancer risk: a review of the epidemiologic literature. European Journal of Cancer Prevention. 12:427–430.

26. Boffetta P, Matisane L, Mundt KA, Dell LD. 2003. Meta-analysis of studies of occupational exposure to vinyl chloride in relation to cancer mortality. Scand J Work Environ Health. 29:220-229.

27. Scelo G, Constantinescu V, Csiki I, Zaridze D, et al. 2004. Occupational exposure to vinyl chloride, acrylonitrile and styrene and lung cancer risk (Europe). Cancer Causes Control. 15:445-452.

28. Grosse Y, Baan R, Straif K, Secretan B, et al. 2007. Carcinogenicity of 1,3-butadiene, ethylene oxide, vinyl chloride, vinyl fluoride, and vinyl bromide. Oncology: The Lancet. 8:679-680.

29. Calvert GM, Ruder AM, Petersen MR. 2010. Mortality and end-stage renal disease incidence among dry cleaning workers. OEM [Epub ahead of print, Dec 16, 2010]

30. U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program 2005. Report on Carcinogens, Eleventh Edition.

31. Mundt KA, Birk T, Burch MT. 2003. Critical review of the epidemiological literature on occupational exposure to perchloroethylene and cancer. Int Arch Occup Environ Health. 76:473-91.

32. Cooper GS, Makris SL, Nietert PJ, Jinot J. 2009. Evidence of Autoimmune-Related Effects of Trichloroethylene Exposure from Studies in Mice and Humans. Environ Health Perspect 117:696–702.

You can find more information in:

EPA and tetrachloroethylene (perchloroethylene)

Hazard Summary-Created in April 1992; Revised in January 2000

Tetrachloroethylene is widely used for dry-cleaning fabrics and metal degreasing operations. The main effects of tetrachloroethylene in humans are neurological, liver, and kidney effects following acute (short-term) and chronic (long-term) inhalation exposure. Adverse reproductive effects, such as spontaneous abortions, have been reported from occupational exposure to tetrachloroethylene; however, no definite conclusions can be made because of the limitations of the studies. Results from epidemiological studies of dry-cleaners occupationally exposed to tetrachloroethylene suggest increased risks for several types of cancer. Animal studies have reported an increased incidence of liver cancer in mice, via inhalation and gavage (experimentally placing the chemical in the stomach), and kidney and mononuclear cell leukemia in rats. In the mid-1980s,

EPA considered the epidemiological and animal evidence on tetrachloroethylene as intermediate between a probable and possible human carcinogen (Group B/C). The Agency is currently reassessing its potential carcinogenicity.

Please Note: The main sources of information for this fact sheet are EPA’s Integrated Risk Information System (IRIS), which contains information on oral chronic toxicity and the RfD, and the Agency for Toxic Substances and Disease Registry’s (ATSDR’s) Toxicological Profile for Tetrachloroethylene. Another secondary source is EPA’s Health Effects Assessment for Tetrachloroethylene.

Uses

• Tetrachloroethylene is used for dry cleaning and textile processing, as a chemical intermediate, and for vapor degreasing in metal-cleaning operations. (1)

Sources and Potential Exposure

• Prior to 1981, tetrachloroethylene was detected in ambient air at average levels of 0.16 parts per billion (ppb) in rural and remote areas, 0.79 ppb in urban and suburban areas, and 1.3 ppb in areas near emission sources. (1)
• Tetrachloroethylene has also been detected in drinking water; one survey prior to 1984 of water supplies from groundwater sources reported a median concentration of 0.75 ppb for the samples in which tetrachloroethylene was detected, with a maximum level of 69 ppb. (1)
• Occupational exposure to tetrachloroethylene may occur, primarily in dry cleaning establishments and at industries manufacturing or using the chemical. (1)

Assessing Personal Exposure

• Tetrachloroethylene can be measured in the breath, and breakdown products of tetrachloroethylene can be measured in the blood and urine. (1)

Health Hazard Information

Acute Effects:

• Effects resulting from acute, inhalation exposure of humans to tetrachloroethylene vapors include irritation of the upper respiratory tract and eyes, kidney dysfunction, and at lower concentrations, neurological effects, such as reversible mood and behavioral changes, impairment of coordination, dizziness, headache, sleepiness, and unconciousness. (1)
• Animal studies have reported effects on the liver, kidney, and central nervous system (CNS) from acute inhalation exposure to tetrachloroethylene. (1)
• Acute animal tests in mice have shown tetrachloroethylene to have low toxicity from inhalation and oral exposure. (1)

Chronic Effects (Noncancer):

• The major effects from chronic inhalation exposure to tetrachloroethylene in humans are neurological effects, including sensory symptoms such as headaches, impairments in cognititve and motor neurobehavioral functioning and color vision decrements. Other effects noted in humans include cardiac arrhythmia, liver damage, and possible kidney effects. (1,5)
• Animal studies have reported effects on the liver, kidney, and CNS from chronic inhalation exposure to tetrachloroethylene. (1,5)
• EPA has not established a Reference Concentration (RfC) for tetrachloroethylene. (4)
• The Reference Dose (RfD) for tetrachloroethylene is 0.01 milligrams per kilogram body weight per day (mg/kg/d) based on hepatotoxicity in mice and weight gain in rats. The RfD is an estimate (with uncertainty spanning perhaps an order of magnitude) of a daily oral exposure to the human population (including sensitive subgroups) that is likely to be without appreciable risk of deleterious noncancer effects during a lifetime. It is not a direct estimator of risk, but rather a reference point to gauge the potential effects. At exposures increasingly greater than the RfD, the potential for adverse health effects increases. Lifetime exposure above the RfD does not imply that an adverse health effect would necessarily occur. (4)
• EPA has medium confidence in the RfD based on low confidence in the study on which the RfD was based due to the lack of complete histopathological examination at the no-observed-adverse-effect level (NOAEL) in the mouse; and medium confidence in the database because it is relatively complete but lacks studies of reproductive and teratology endpoints subsequent to oral exposure. (4)
• ATSDR has calculated a chronic-duration inhalation minimal risk level (MRL) of 0.04 parts per million (ppm) (0.3 milligrams per cubic meter, mg/m³) for tetrachloroethylene based on neurological effects in humans. The 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. (1)
• Repeated skin contact may cause irritation. (1)

Reproductive/Developmental Effects:

• Some adverse reproductive effects, such as spontaneous abortions, menstrual disorders, altered sperm structure, and reduced fertility, have been reported in studies of workers occupationally exposed to tetrachloroethylene. However, no definitive conclusions can be made because of the limitations of the studies. (1)
• In one study of residents exposed to drinking water contaminated with tetrachloroethylene and other solvents, there was a suggestion that birth defects were associated with exposure. However, no firm conclusions can be drawn from this study due to multiple chemical exposures and problems with the analysis. (1)
• Increased fetal resorptions and effects to the fetus have been reported in animals exposed to high levels of tetrachloroethylene by inhalation. (1)

Cancer Risk:

• Epidemiological studies of dry cleaning workers exposed to tetrachloroethylene and other solvents suggest an increased risk for a variety of cancers (esophagus, kidney, bladder, lung, pancreas, and cervix). These studies are complicated by potential exposure to other chemicals and personal lifestyle factors such as alcohol consumption and smoking were not taken into account. (1,5,6)
• One human study reported that there was a potential association between drinking water contaminated with tetrachloroethylene and other chemicals and an increased risk of childhood leukemia. The statistical significance of the incidence of leukemia has not been resolved. (1)
• Animal studies have reported an increased incidence of liver tumors in mice, from inhalation and gavage (experimentally placing the chemical in the stomach) exposure, and kidney and mononuclear cell leukemias in rats, via inhalation exposure. (1,5,6)
• Less than 5 percent of absorbed tetrachloroethylene is metabolized by humans to trichloroacetic acid (TCA), with the remainder being exhaled unchanged. TCA is classified as a Group C, possible human carcinogen based on limited evidence of liver tumors in mice (but not rats). (4,7)
• EPA does not currently have a classification for the carcinogenicity of tetrachloroethylene. The International Agency for Research on Cancer (IARC) has classified tetrachloroethylene as probably carcinogenic to humans.
• EPA uses mathematical models, based on animal studies, to estimate the probability of a person developing cancer from breathing air containing a specified concentration of a chemical. EPA has calculated a provisional inhalation unit risk estimate of 5.8 × 10^-7 (µg/m³)^-1. A provisonal value is one which has not received Agency-wide review. (7)
• EPA has calculated a provisional oral cancer slope factor of 0.051 (mg/kg/d)^-1. (5)

Physical Properties

• Tetrachloroethylene is a nonflammable colorless liquid with a sharp sweet odor; the odor threshold is 1 ppm. (1)
• The chemical formula for tetrachloroethylene is C₂Cl₄, and the molecular weight is 165.83 g/mol. (1)
• The vapor pressure for tetrachloroethylene is 18.47 mm Hg at 25 °C, and it has a log octanol/water partition coefficient (log K_ow) of 3.40. (1)

Conversion Factors:
To convert concentrations in air (at 25°C) from ppm to mg/m³: mg/m³ = (ppm) × (molecular weight of the compound)/(24.45). For tetrachloroethylene: 1 ppm = 6.78 mg/m³. To convert concentrations in air from µg/m³ to mg/m³: mg/m³ = (µg/m³) × (1 mg/1,000 µg).

AIHA ERPG–American Industrial Hygiene Association’s emergency response planning guidelines. ERPG 1 is the maximum airborne concentration below which it is believed nearly all individuals could be exposed up to one hour without experiencing other than mild transient adverse health effects or perceiving a clearly defined objectionable odor; ERPG 2 is the maximum airborne concentration below which it is believed nearly all individuals could be exposed up to one hour without experiencing or developing irreversible or other serious health effects that could impair their abilities to take protective action.
ACGIH STEL–American Conference of Governmental and Industrial Hygienists’ short-term exposure limit; 15-min time-weighted-average exposure that should not be exceeded at any time during a workday even if the 8-h time-weighted-average is within the threshold limit value.
ACGIH TLV–American Conference of Governmental and Industrial Hygienists’ threshold limit value expressed as a time-weighted average; the concentration of a substance to which most workers can be exposed without adverse effects.
LC₅₀ (Lethal Concentration₅₀)–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.
NIOSH IDLH– National Institute of Occupational Safety and Health’s immediately dangerous to life or health concentration; NIOSH recommended exposure limit to ensure that a worker can escape from an exposure condition that is likely to cause death or immediate or delayed permanent adverse health effects or prevent escape from the environment.
OSHA PEL–Occupational Safety and Health Administration’s permissible exposure limit expressed as a time-weighted average; the concentration of a substance to which most workers can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.

The health and regulatory values cited in this factsheet were obtained in December 1999.
^a Health numbers are toxicological numbers from animal testing or risk assessment values developed by EPA.
^b Regulatory numbers are values that have been incorporated in Government regulations, while advisory numbers are nonregulatory values provided by the Government or other groups as advice. OSHA numbers are regulatory, whereas NIOSH, ACGIH, and AIHA numbers are advisory.
^cThe LOAEL is from the critical study used as the basis for the ATSDR chronic inhalation MRL.

References

1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for Tetrachloroethylene (Update). U.S. Public Health Service, U.S. Department of Health and Human Services, Atlanta, GA. 1997.
2. American Conference of Governmental and Industrial Hygienists (ACGIH). 1999 TLVs and BEIs: Threshold Limit Values for Chemical Substances and Physical Agents, Biological Exposure Indices. Cincinnati, OH. 1999.
3. Occupational Safety and Health Administration (OSHA). Occupational Safety and Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations 29 CFR 1910.1000. 1998.
4. U.S. Environmental Protection Agency. Integrated Risk Information System (IRIS) on Tetrachloroethylene. National Center for Environmental Assessment, Office of Research and Development, Washington, DC. 1999.
5. U.S. Environmental Protection Agency. Health Effects Assessment for Tetrachloroethylene. EPA/600/8-89-096. Environmental Criteria and Assessment Office, Office of Health and Environmental Assessment, Office of Research and Development, Cincinnati, OH. 1988.
6. U.S. Environmental Protection Agency. Updated Health Assessment Document for Tetrachloroethylene. EPA/600/8-82/005B. Environmental Criteria and Assessment Office, Office of Health and Environmental Assessment, Office of Research and Development, Cincinnati, OH. 1988.
7. U.S. Environmental Protection Agency. Risk Assessment Issue Paper for Carcinogenicity Information for Tetrachloroethylene (Perchloroethylene, PERC) (CASRN 127-18-4). Superfund Technical Support Center, National Center for Environmental Assessment, Cincinnati, OH. nd.
8. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to Chemical Hazards. U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.
9. American Industrial Hygiene Association (AIHA). The AIHA 1998 Emergency Response Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook. 1998.
10. U.S. Environmental Protection Agency. National Emission Standards for Hazardous Air Pollutants: Wood Furniture Manufacturing Operations. Federal Register 63 FR 34336-346. June 24, 1998.

Tetrachloroethylene, also known under its systematic name tetrachloroethene and many other names, is a chlorocarbon with the formula Cl₂C=CCl₂. It is a colourless liquid widely used for dry cleaning of fabrics, hence it is sometimes called “dry-cleaning fluid.” It has a sweet odor detectable by most people at a concentration of 1 part per million (1 ppm). Worldwide production was about 1 megatonne in 1985.^[1]

Production

Michael Faraday first synthesized tetrachloroethylene in 1821 by thermal decomposition of hexachloroethane.

C₂Cl₆ → C₂Cl₄ + Cl₂

Most tetrachloroethene is produced by high temperature chlorinolysis of light hydrocarbons. The method is related to Faraday’s discovery since hexachloroethane is generated and thermally decomposes.^[1] Side products include carbon tetrachloride, hydrogen chloride, and hexachlorobutadiene.

Several other methods have been developed. When 1,2-dichloroethane is heated to 400 °C with chlorine, tetrachloroethene is produced by the chemical reaction:

ClCH₂CH₂Cl + 3 Cl₂ → Cl₂C=CCl₂ + 4 HCl

This reaction can be catalyzed by a mixture of potassium chloride and aluminium chloride or by activated carbon. Trichloroethylene is a major byproduct, which is separated by distillation.

According to an EPA report of 1976, the quantity of Tetrachloroethylene (also known as perchloroethylene or PCE) produced in the United States in just one year 1973, totaled 706 million pounds (320,000 metric tons). Diamond Shamrock, Dow Chemical Company, E.I DuPont and Vulcan Materials Company (Chemical Division) were among the top eight producers nationwide. ^[2]

Uses

Tetrachloroethylene is an excellent solvent for organic materials. Otherwise it is volatile, highly stable, and nonflammable. For these reasons, it is widely used in dry cleaning. Usually as a mixture with other chlorocarbons, it is also used to degrease metal parts in the automotive and other metalworking industries. It appears in a few consumer products including paint strippers and spot removers.

Historical applications

Tetrachloroethene was once extensively used as an intermediate in the manufacture of HFC-134a and related refrigerants. In the early 20th century, tetrachloroethene was used for the treatment for hookworm infestation.^[3]

Health and safety

The International Agency for Research on Cancer has classified tetrachloroethene as a Group 2A carcinogen, which means that it is probably carcinogenic to humans.^[4] Like many chlorinated hydrocarbons, tetrachloroethene is a central nervous system depressant and can enter the body through respiratory or dermal exposure.^[5] Tetrachloroethene dissolves fats from the skin, potentially resulting in skin irritation.

Animal studies and a study of 99 twins by Dr. Samuel Goldman and researchers at the Parkinson’s Institute in Sunnyvale, California determined there is a “lot of circumstantial evidence” that exposure to tetrachloroethene increases the risk of developing Parkinson’s disease ninefold. Larger population studies are planned.^[6]

At temperatures over 600 °F (316 °C), such as in welding, tetrachloroethylene can decompose into phosgene, an extremely poisonous gas.^[7][8] Tetrachloroethylene should not be used near welding operations, flames, or hot surfaces.^[9]

Testing for exposure

Tetrachloroethene exposure can be evaluated by a breath test, analogous to breath-alcohol measurements. Because it is stored in the body’s fat and slowly released into the bloodstream, tetrachloroethene can be detected in the breath for weeks following a heavy exposure. Tetrachloroethylene and trichloroacetic acid (TCA), a breakdown product of tetrachloroethene, can be detected in the blood.

In Europe, the Scientific Committee on Occupational Exposure Limits (SCOEL) recommends for tetrachloroethylene an occupational exposure limit (8h time-weighted average) of 20 ppm and a short-term exposure limit (15 min) of 40 ppm.^[10]

Environmental contamination

Tetrachloroethene is a common soil contaminant. With a specific gravity greater than 1, tetrachloroethylene will be present as a dense nonaqueous phase liquid if sufficient quantities of liquid are spilled in the environment. Because of its mobility in groundwater, its toxicity at low levels, and its density (which causes it to sink below the water table), cleanup activities are more difficult than for oil spills. Recent research has focused on the in place remediation of soil and ground water pollution by tetrachloroethylene. Instead of excavation or extraction for above-ground treatment or disposal, tetrachloroethylene contamination has been successfully remediated by chemical treatment or bioremediation. Bioremediation has been successful under anaerobic conditions by reductive dechlorination by Dehalococcoides sp. and under aerobic conditions by cometabolism by Pseudomonas sp.^[11][12] Partial degradation daughter products include trichloroethylene, cis-1,2-dichloroethene and vinyl chloride; full degradation converts tetrachloroethylene to ethene and hydrogen chloride dissolved in water.

Estimates state that 85% of tetrachloroethylene produced is released into the atmosphere; while models from OECD assumed that 90% is released into the air and 10% to water. Based on these models, its distribution in the environment is estimated to be in the air (76.39% – 99.69%), water (0.23% – 23.2%), soil (0.06-7%), with the remainder in the sediment and biota. Estimates of lifetime in the atmosphere vary, but a 1987 survey estimated the lifetime in the air has been estimated at about 2 months in the Southern Hemisphere and 5–6 months in the Northern Hemisphere. Degradation products observed in a laboratory include phosgene, trichloroacetyl chloride, hydrogen chloride, carbon dioxide, and carbon monoxide. Tetrachloroethylene is degraded by hydrolysis, and is also persistent under aerobic conditions. This compound is degraded by reductive dechlorination with anaerobic conditions present, with the degradation products like trichloroethene, dichloroethene, vinyl chloride, ethene, and ethane.^[13]

References

Further reading

• “Toxicological Profile for Tetrachloroethene”. Agency for Toxic Substances and Disease Registry. 1997.

• Doherty, R.E. (2000). “A History of the Production and Use of Carbon Tetrachloride, Tetrachloroethylene, Trichloroethylene and 1,1,1-Trichloroethane in the United States: Part 1 – Historical Background; Carbon Tetrachloride and Tetrachloroethylene”. Environmental Forensics 1 (2): 69–81. DOI:10.1006/enfo.2000.0010.

External links

• ATSDR Case Studies in Environmental Medicine: Tetrachloroethylene Toxicity U.S. Department of Health and Human Services
• Australian National Pollutant Inventory (NPI) page
• “Toxic Fumes May Have Made Gunman Snap”, by Julian Kesner, New York Daily News, April 20, 2007.

67-66-3

Hazard Summary-Created in April 1992; Revised in January 2000

Chloroform may be released to the air as a result of its formation in the chlorination of drinking water, wastewater and swimming pools. Other sources include pulp and paper mills, hazardous waste sites, and sanitary landfills. The major effect from acute (short-term) inhalation exposure to chloroform is central nervous system depression. Chronic (long-term) exposure to chloroform by inhalation in humans has resulted in effects on the liver, including hepatitis and jaundice, and central nervous system effects, such as depression and irritability. Chloroform has been shown to be carcinogenic in animals after oral exposure, resulting in an increase in kidney and liver tumors. EPA has classified chloroform as a Group B2, probable human carcinogen.

Please Note: The main sources of information for this fact sheet are EPA’s Integrated Risk Information System (IRIS), which contains information on oral chronic toxicity and the RfD, and the carcinogenic effects of chloroform including the unit cancer risk for inhalation exposure, and the Agency for Toxic Substances and Disease Registry’s (ATSDR’s) Toxicological Profile for Chloroform.

Uses

• The vast majority of the chloroform produced in the United States is used to make HCFC-22. The rest is produced for export and for miscellaneous uses. (1)
• Chloroform was used in the past as an extraction solvent for fats, oils, greases, and other products; as a dry cleaning spot remover; in fire extinguishers; as a fumigant; and as an anesthetic. However, chloroform is no longer used in these products. (1)

Sources and Potential Exposure

• Chloroform may be released to the air from a large number of sources related to its manufacture and use, as well as its formation in the chlorination of drinking water, wastewater, and swimming pools. Pulp and paper mills, hazardous waste sites, and sanitary landfills are also sources of air emissions. The background level of chloroform in ambient air in the early 1990s was estimated at 0.00004 parts per million (ppm). (1)
• Human exposure to chloroform may occur through drinking water, where chloroform is formed as a result of the chlorination of naturally occurring organic materials found in raw water supplies. Measurements of chloroform in drinking water during the 1970s and 1980s ranged from 0.022 to 0.068 ppm. (1)
• Chloroform may also be found in some foods and beverages, largely from the use of tap water during production processes. (1)

Assessing Personal Exposure

• Chloroform can be detected in blood, urine, and body tissues. However, these methods are not very reliable because chloroform is rapidly eliminated from the body, and the tests are not specific for chloroform. (1)

Health Hazard Information

Acute Effects:

• The major effect from acute inhalation exposure to chloroform in humans is central nervous system depression. At very high levels (40,000 ppm), chloroform exposure may result in death, with concentrations in the range of 1,500 to 30,000 ppm producing anesthesia, and lower concentrations (<1,500 ppm) resulting in dizziness, headache, tiredness, and other effects. (1,2)
• Effects noted in humans exposed to chloroform via anesthesia include changes in respiratory rate, cardiac effects, gastrointestinal effects, such as nausea and vomiting, and effects on the liver and kidney. Chloroform is not currently used as a surgical anesthetic. (1,2)
• In humans, a fatal oral dose of chloroform may be as low as 10 mL (14.8 g), with death due to respiratory or cardiac arrest. (1,2)
• Tests involving acute exposure of animals have shown chloroform to have low acute toxicity from inhalation exposure and moderate acute toxicity from oral exposure. (3)

Chronic Effects (Noncancer):

• Chronic exposure to chloroform by inhalation in humans is associated with effects on the liver, including hepatitis and jaundice, and central nervous system effects, such as depression and irritability. Inhalation exposures of animals have also resulted in effects on the kidney. (1,2)
• Chronic oral exposure to chloroform in humans has resulted in effects on the blood, liver, and kidney. (1,2)
• EPA has not established a Reference Concentration (RfC) for chloroform. (4)
• The California Environmental Protection Agency (CalEPA) has established a chronic reference exposure level of 0.3 milligrams per cubic meter (mg/m³) for chloroform based on exposures resulting in kidney and liver effects in rats. The CalEPA reference exposure level is a concentration at or below which adverse health effects are not likely to occur. It is not a direct estimator of risk, but rather a reference point to gauge the potential effects. At lifetime exposures increasingly greater than the reference exposure level, the potential for adverse health effects increases. (5)
• ATSDR has established an acute inhalation minimal risk level (MRL) of 0.5 mg/m³ (0.1 ppm) based on exposures resulting in liver effects in mice, an intermediate inhalation MRL of 0.2 mg/m³ (0.05 ppm) based on worker exposures resulting in liver effects in humans, and a chronic inhalation MRL of 0.1 mg/m³ (0.02 ppm) also based on liver effects in humans. The 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. (1)
• The Reference Dose (RfD) for chloroform is 0.01 milligrams per kilogram per day (mg/kg/d) based on exposures resulting in fatty cyst formation in the livers of dogs. The RfD is an estimate (with uncertainty spanning perhaps an order of magnitude) of a daily oral exposure to the human population (including sensitive subgroups) that is likely to be without appreciable risk of deleterious noncancer effects during a lifetime. (4)
• EPA has medium to low confidence in the RfD due to: medium confidence in the critical study on which the RfD was based because only two treatment doses were used, and a no-observed-effect level (NOEL) was not determined; and medium to low confidence in the database because several studies support the choice of a lowest-observed-adverse-effect level (LOAEL), but a NOEL was not found. (4)

Reproductive/Developmental Effects:

• Little information is available on the reproductive or developmental effects of chloroform in humans, via any route of exposure. A possible association between certain birth outcomes (e.g., low birth weight, cleft palate) and consumption of contaminated drinking water was reported. However, because multiple contaminants were present, the role of chloroform is unclear. (1)
• Animal studies have demonstrated developmental effects, such as decreased fetal body weight, fetal resorptions, and malformations in the offspring of animals exposed to chloroform via inhalation. (1)
• Reproductive effects, such as decreased conception rates, decreased ability to maintain pregnancy, and an increase in the percentage of abnormal sperm were observed in animals exposed to chloroform through inhalation. (1)
• Animal studies have noted decreased fetal weight, increased fetal resorptions, but no evidence of birth defects, in animals orally exposed to chloroform. (1)

Cancer Risk:

• No information is available regarding cancer in humans or animals after inhalation exposure to chloroform. (1)
• Epidemiologic studies suggest an association between cancer of the large intestine, rectum, and/or bladder and the constituents of chlorinated drinking water, including chloroform. However, there are no epidemiologic studies of water containing only chloroform. (1)
• Chloroform has been shown to be carcinogenic in animals after oral exposure, resulting in an increase in kidney and liver tumors. (1)
• EPA considers chloroform to be a probable human carcinogen and has ranked it in EPA’s Group B2. (4)
• EPA has determined that although chloroform is likely to be carcinogenic to humans by all routes of exposure under high-exposure conditions that lead to cell death and regrowth in susceptible tissues, chloroform is not likely to cause cancer in humans by any route of exposure under exposure conditions that do not cause cell death and regrowth. Therefore, EPA has not derived either an oral carcinogenic potency slope or an inhalation unit risk for chloroform.

Physical Properties

• Chloroform is a colorless liquid that is not very soluble in water and is very volatile. (1,6)
• Chloroform has a pleasant, nonirritating odor; the odor threshold is 85 ppm. (1)
• The chemical formula for chloroform is CHCl₃, and it has a molecular weight of 119.38 g/mol. (1)
• The vapor pressure for chloroform is 159 mm Hg at 20 °C, and it has a log octanol/water partition coefficient (log K_ow) of 1.97. (1)

Conversion Factors:
To convert concentrations in air (at 25°C) from ppm to mg/m³: mg/m³ = (ppm) × (molecular weight of the compound)/(24.45). For chloroform: 1 ppm = 4.88 mg/m³. To convert concentrations in air from µg/m³ to mg/m³: mg/m³ = (µg/m³) × (1 mg/1,000 µg).

ACGIH TLV–American Conference of Governmental and Industrial Hygienists’ threshold limit value expressed as a time-weighted average; the concentration of a substance to which most workers can be exposed without adverse effects.
LC₅₀ (Lethal Concentration₅₀)–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.
NIOSH REL–National Institute of Occupational Safety and Health’s recommended exposure limit; NIOSH-recommended exposure limit for an 8- or 10-h time-weighted-average exposure and/or ceiling.
OSHA PEL–Occupational Safety and Health Administration’s permissible exposure limit expressed as a time-weighted average; the concentration of a substance to which most workers can be exposed without adverse effect averaged over a normal 8-h workday or a 40-h workweek.

The health and regulatory values cited in this factsheet were obtained in December 1999.
^aHealth numbers are toxicological numbers from animal testing or risk assessment values developed by EPA.
^b Regulatory numbers are values that have been incorporated in Government regulations, while advisory numbers are nonregulatory values provided by the Government or other groups as advice. OSHA numbers are regulatory, whereas NIOSH and ACGIH numbers are advisory.
^cThese cancer risk estimates were derived from oral data and converted to provide the estimated inhalation risk.
^dThe LOAEL is from the critical study used as the basis for the CalEPA chronic reference exposure level.

References

1. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for Chloroform. Public Health Service, U.S. Department of Health and Human Services, Atlanta, GA. 1997.
2. U.S. Department of Health and Human Services. Hazardous Substances Data Bank (HSDB, online database). National Toxicology Information Program, National Library of Medicine, Bethesda, MD. 1993.
3. U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical Substances (RTECS, online database). National Toxicology Information Program, National Library of Medicine, Bethesda, MD. 1993.
4. U.S. Environmental Protection Agency. Integrated Risk Information System (IRIS) on Chloroform. National Center for Environmental Assessment, Office of Research and Development, Washington, DC. 1999.
5. California Environmental Protection Agency (CalEPA). Technical Support Document for the Determination of Noncancer Chronic Reference Exposure Levels. Draft for Public Comment. Office of Environmental Health Hazard Assessment, Berkeley, CA. 1997.
6. The Merck Index. An Encyclopedia of Chemicals, Drugs, and Biologicals. 11th ed. Ed. S. Budavari. Merck and Co. Inc., Rahway, NJ. 1989.
7. Occupational Safety and Health Administration (OSHA). Occupational Safety and Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations. 29 CFR 1910.1000. 1998.
8. American Conference of Governmental Industrial Hygienists (ACGIH). 1999 TLVs and BEIs. Threshold Limit Values for Chemical Substances and Physical Agents. Biological Exposure Indices. Cincinnati, OH. 1999.
9. National Institute for Occupational Safety and Health (NIOSH). Pocket Guide to Chemical Hazards. U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention. Cincinnati, OH. 1997.

Nitrate Facts

Nitrates in Drinking Water / by J.R. Self and R.M. Waskom / Colorado State University (10/08)1

Quick Facts…

Nitrate is a colorless, odorless, and tasteless compound that is present in some groundwater in Colorado.

Nitrate can be expressed as either NO3 (nitrate) or NO3-N (nitrate-nitrogen). Nitrate levels above the EPA Maximum Contaminant Level of 10mg/l NO3- N or 45 mg/l NO3 may cause methemoglobinemia in infants.

Proper management of fertilizers, manures, and other nitrogen sources can minimize contamination of drinking water supplies.

Nitrate (NO3) is a naturally occurring form of nitrogen found in soil. Nitrogen is essential to all life. Most crop plants require large quantities to sustain high yields.

The formation of nitrates is an integral part of the nitrogen cycle in our environment. In moderate amounts, nitrate is a harmless constituent of food and water. Plants use nitrates from the soil to satisfy nutria.nt requirements and may accumulate nitrate in their leaves and stems. Due to its high mobility, nitrate also can leach into groundwater. If people or animals drink water high in nitrate, it may cause methemoglobinemia, an illness found especially in infants.

Nitrates form when microorganisms break down fertilizers, decaying plants, manures or other organic residues. Usually plants take up these nitrates, but sometimes rain or irrigation water can leach them into groundwater. Although nitrate occurs naturally in some groundwater, in most cases higher levels are thought to result from human activities. Common sources of nitrate include:

fertilizers and manure,

animal feedlots,

municipal wastewater and sludge,

septic systems, and

N-fixation from atmosphere by legumes, bacteria and lightning.

Health Effect of Nitrates

People

High nitrate levels in water can cause methemoglobinemia or blue baby syndrome, a condition found especially in infants under six months. The stomach acid of an infant is not as strong as in older children and adults. This causes an increase in bacteria that can readily convert nitrate to nitrite (NO2). Do not let infants drink water that exceeds 10 mg/l NO3-N. This includes formula preparation.

Nitrite is absorbed in the blood, and hemoglobin (the oxygen-carrying component of blood) is converted to methemoglobin. Methemoglobin does not carry oxygen efficiently. This results in a reduced oxygen supply to vital tissues such as the brain. Methemoglobin in infant blood cannot change back to hemoglobin, which normally occurs in adults. Severe methemoglobinemia can result in brain damage and death.

Pregnant women, adults with reduced stomach acidity, and people deficient in the enzyme that changes methemoglobin back to normal hemoglobin are all susceptible to nitrite-induced methemoglobinemia. The most obvious symptom of methemoglobinemia is a bluish color of the skin, particularly around the eyes and mouth. Other symptoms include headache, dizziness, weakness or difficulty in breathing. Take babies with the above symptoms to the hospital emergency room immediately. If recognized in time, methemoglobinemia is treated easily with an injection of methylene blue.

Healthy adults can consume fairly large amounts of nitrate with few known health effects. In fact, most of the nitrate we consume is from our diets, particularly from raw or cooked vegetables. This nitrate is readily absorbed and excreted in the urine. However, prolonged intake of high levels of nitrate are linked to gastric problems due to the formations of nitrosamines. N-nitrosamine compounds have been shown to cause cancer in test animals. Studies of people exposed to high levels of nitrate or nitrite have not provided convincing evidence of an increased risk of cancer.

Animals

Although there is no enforceable drinking water standard for livestock, do not allow animals to drink water with more than 100 mg/l NO3-N. This is especially true of young animals. They are affected by nitrates the same way as human babies. Older animals may tolerate higher levels.

Ruminant animals (cattle, sheep) are susceptible to nitrate poisoning because bacteria present in the rumen convert nitrate to nitrite. Nonruminant animals (swine, chickens) rapidly eliminate nitrate in their urine. Horses are monogastric, but their large cecum acts much like a rumen. This makes them more susceptible to nitrate poisoning than other monogastric animals.

It is difficult to determine the toxicity of nitrate in animals because it depends on the rate at which the substance is consumed. A few hundred milligrams of nitrate may cause poisoning if consumed in a few hours. But spread over a whole day, 1,000 mg nitrate may cause no signs of toxicity.

Common symptoms include abdominal pain, diarrhea, muscular weakness or poor coordination. Affected animals will have blood that is a chocolate-brown color. If the problem is diagnosed in time, they can fully recover with a treatment of methylene blue. Pregnant animals may abort within a few days.

Nitrate also exists in animal feeds and fodder. Drought-stressed forage plants commonly have high nitrate levels. These feeds can have an additive effect when consumed with high nitrate drinking water.

The drinking water standard

Reports of methemoglobinemia are extremely rare. Clinical infant methemoglobinemia was first recognized in 1945. About 2,000 cases were reported in North America and Europe by 1971. Fatality rates were reported to be approximately 7 to 8 percent. From 1960 to 1972, however, only one death from blue baby syndrome was documented.

Methemoglobinemia has not been reported where water contains less than 10 mg/l of NO3-N. This level has been adopted by the U.S. Environmental Protection Agency as the standard in the Primary Drinking Water Regulations, chiefly to protect young infants.

Nitrate values are commonly reported as either nitrate (NO3) or as nitrate-nitrogen (NO3-N). The maximum contaminant level (MCL) in drinking water as nitrate (NO3) is 45 mg/l, whereas the MCL as NO3-N is 10 mg/l.

The MCL is the highest level of NO3 or NO3-N that is allowable in public drinking water supplies by the U.S. Environmental Protection Agency (EPA). These figures also may be reported in ppm (parts per million), which is equivalent to mg/l. Be sure you know which value is reported for your water sample.

Protecting your drinking water

The 1990 EPA National Survey of Drinking Water Wells found that approximately 57 percent of the private wells tested contained detectable levels of nitrates. However, only 2.4 percent exceeded the EPA maximum contaminant level. In Colorado, nitrate contamination above the MCL occurs mainly in rural areas overlying vulnerable aquifers.

Protecting your drinking water supply from contamination is important for health and to protect property values and minimize potential liability. High nitrate levels often are associated with poorly constructed or improperly located wells. Locate new wells uphill and at least 100 feet away from feedlots, septic systems, barnyards and chemical storage facilities. Properly seal or cap abandoned wells.

Manage nonpoint sources of water pollution (fields, lawns) to limit the loss of excess water and plant nutrients. Match fertilizer and irrigation applications to precise crop uptake needs in order to minimize groundwater contamination.

Best management practices for fertilizer use

Careful fertilizer management can reduce nitrate leaching to groundwater. Consider the following practices in planning your fertilizer program:

Use soil and water analysis to determine exact nitrogen needs of crop (see fact sheet 0.500, Soil Sampling).

Set a realistic yield goal for each field. Take the five-year average production of your field and add 5 percent to get an attainable yield goal.

Credit all sources of nitrogen available to the crop, including manures, water, organic matter, legumes and residual subsoil nitrate.

Water quality analysis

Nitrate is a tasteless, colorless and odorless compound that you cannot detect unless your water is chemically analyzed. If you drink water from a private well, get a qualified laboratory to test it yearly. The local health department or Colorado State University Extension county office usually can supply the name of an approved testing laboratory in your area.

Sample water for nitrate testing at the well site or at a tap inside the house. Place samples in clean, 4- to 16-ounce plastic containers. Send the sample to a laboratory immediately. Refrigerating it will help keep it intact until it reaches a laboratory. Do not freeze it.

Laboratory results will be compared to the MCL, and recommendations for treatment should be considered if nitrate levels exceed 10 mg/l NO3-N. Be aware that nitrate levels in groundwater may vary seasonally. If your water tests high or borderline high, retest your water every three to six months.

Purification of contaminated water

While it may be technically possible to treat contaminated groundwater, it can be difficult, expensive and not totally effective. For this reason, prevention is the best way to ensure clean water. Water treatments include distillation, reverse osmosis, ion exchange or blending.

Distillation boils the water, catches the resulting steam, and condenses the steam on a cold surface (a condenser). Nitrates and other minerals remain behind in the boiling tank.

Reverse osmosis forces water under pressure through a membrane that filters out minerals and nitrate. One-half to two-thirds of the water remains behind the membrane as rejected water. Higher-yield systems use water pressures of 150 psi.

Ion-exchange takes another substance, such as chloride, and trades places with nitrate. An ion exchange unit is filled with special resin beads that are charged with chloride. As water passes over the beads, the resin takes up nitrate in exchange for chloride. As more water passes over the resin, all the chloride is exchanged for nitrate. The resin is recharged by backwashing with sodium chloride solution. The backwash solution, which is high in nitrate, must be properly disposed of.

Blending is another method to reduce nitrates in drinking water. Mix contaminated water with clean water from another source to lower overall nitrate concentration. Blended water is not safe for infants but is acceptable for livestock and healthy adults.

Charcoal filters and water softeners do not adequately remove nitrates from water. Boiling nitrate-contaminated water does not make it safe to drink and actually increases the concentration of nitrates. Drilling a new well to deeper water with less nitrate may be a feasible remedy in certain areas. In many cases, the most effective alternative is to use bottled water for drinking and cooking.

Glossary

Blue baby syndrome: A disease that affects the oxygen carrying capacity of infant’s blood, usually resulting from the consumption of high levels of NO3. Also known as methemoglobinemia.

Contaminant: Any physical, chemical, biological or radiological substance that degrades water quality.

Groundwater: Water that saturates subsurface formations or aquifers.

Leaching: The downward movement of dissolved or suspended minerals, fertilizers, agricultural chemicals or other substances through the soil.

Maximum contaminant level (MCL): The highest amount of a specific contaminant allowed by the EPA in public drinking water supplies. These are health-based standards that by law must be set as close to the “no-risk” level as feasible.

Nitrate (NO3): An important plant nutrient that is soluble in water and may cause health problems if consumed in large amounts.

Nitrate-nitrogen (NO3-N): Relates to the actual nitrogen in nitrate. Multiply NO3-N values by 4.4 to convert to nitrate.

Nonpoint source pollution: Water contamination from diffuse sources such as agricultural fields, urban runoff or large construction sites.

Parts per million (ppm): A unit of proportion used to describe the concentration of a chemical in water. Equivalent to mg/l.

References

Additional information on water quality can be obtained from the following fact sheets, published by Colorado State University Extension:

J. R. Self. 1998. Domestic Water Quality Criteria. 0.513.

Kendall, P. 1992. Drinking Water Quality. 9.307.

Self, J. R., and P. N. Soltanpour. 1997. Soil Sampling. 0.500.

Soltanpour, P. N., I. Broner, and R. H. Follett. 1999. Nitrogen and Irrigation Management. 0.514.

Soltanpour, P. N. and W. L. Raley. 1993. Livestock Drinking Water Quality. 4.908.

Stanton, T. L. 1992. Nitrate Poisoning. 1.610.

1J.R. Self, Colorado State University Soils Testing Laboratory manager; and R.M. Waskom, Colorado State Extension water quality specialist; soil and crop sciences. 7/95. Reviewed 10/08.

http://www.ext.colostate.edu/pubs/crops/00517.html

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