Part of Air, A WELLography™
First Edition
International Well Building Institute

Table of Contents


Copyright© 2017 International WELL Building Institute PBC. All rights reserved.

International WELL Building Institute PBC authorizes personal use of this Materials WELLography™, which includes the ability by the user to download and print a single copy of the Materials WELLography™ for the user’s own education and reference. In exchange for this authorization, the user agrees:

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Unauthorized use of the Materials WELLography™ violates copyright, trademark, and other laws and is prohibited.


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The International WELL Building Institute (IWBI) and Delos Living LLC (Delos) acknowledge the work of the following IWBI and Delos technical staff that developed and created the WELLographies: Oriah Abera; Niklas Garrn; Trevor Granger; Soyoung Hwang; Michelle Martin; Vienna McLeod; Anja Mikic; Renu Nadkarni; Brendan O’Grady; Chris Ramos; Eric Saunders; Sara Scheineson; Nathan Stodola; Regina Vaicekonyte; Sarah Welton; Kylie Wheelock; and Emily Winer.

IWBI also is grateful for the input and insight provided by the following Subject Matter Experts:

Air: Terry Gordon, PhD; Eric Liberda, PhD; Tim McAuley, PhD; Ellen Tohn, MCP

Water: Eric Liberda, PhD; Tim McAuley, PhD; Margret Whittaker, PhD, MPH, CBiol, FSB, ERB, DABT, ToxServices LLC

Nourishment: Sharon Akabas, PhD; Alice H. Lichtenstein, DSc; Barbara Moore, PhD

Light: Chad Groshart, LEED AP BD+C; Samer Hattar, PhD; Steven Lockley, PhD, Consultant, Delos Living LLC and Member, Well Living Lab Scientific Advisory Board, Neuroscientist, Brigham and Women’s Hospital and Associate Professor of Medicine, Harvard Medical School

Fitness: Dr. Karen Lee, MD, MHSc, FRCPC, President & CEO, Dr. Karen Lee Health + Built Environment + Social Determinants Consulting; Jordan Metzl, MD

Thermal Comfort: Alan Hedge, PhD, CPE, CErgHF; David Lehrer, MArch; Caroline Karmann, PhD, MArch

Acoustics: Arline L. Bronzaft, PhD, Professor Emerita of The City University of New York; Charles Salter, PE

Materials: Clayton Cowl, MD; Matteo Kausch, PhD, Cradle to Cradle Products Innovation Institute; Megan Schwarzman, MD, MPH; Margret Whittaker, PhD, MPH, CBiol, FSB, ERB, DABT, ToxServices LLC

Mind: Anjali Bhagra, MBBS; Lisa Cohen, PhD; Keith Roach, MD; John Salamone, PhD; Nelida Quintero, PhD


None of the parties involved in the funding or creation of the WELL Building Standard™ and the WELLographies™, including Delos Living LLC, its affiliates, subsidiaries, members, employees, or contractors, assume any liability or responsibility to the user or any third parties for the accuracy, completeness, or use of or reliance on any information contained in the WELL Building Standard and the WELLographies, or for any injuries, losses, or damages (including, without limitation, equitable relief) arising from such use or reliance.

Although the information contained in the WELL Building Standard and the WELLographies is believed to be reliable and accurate, all materials set forth within are provided without warranties of any kind, either express or implied, including but not limited to warranties of the accuracy or completeness of information or the suitability of the information for any particular purpose.

The WELL Building Standard and the WELLographies are intended to educate and assist building and real estate professionals in their efforts to create healthier work and living spaces, and nothing in the WELL Building Standard and the WELLographies should be considered, or used as a substitute for, medical advice, diagnosis or treatment.

As a condition of use, the user covenants not to sue and agrees to waive and release Delos Living LLC, its affiliates, subsidiaries, members, employees, or contractors from any and all claims, demands, and causes of action for any injuries, losses, or damages (including, without limitation, equitable relief) that the user may now or hereafter have a right to assert against such parties as a result of the use of, or reliance on, the WELL Building Standard and the WELLographies.

Welcome to WELL

The buildings where we live, work, learn and relax have a profound effect on our well-being: how we feel, what we eat and how we sleep at night. By examining our surroundings and our habits, and making key optimizations and changes, we have the power to cultivate spaces that promote wellness, and support efforts to live healthier, active, mindful lives – a right for every human.

The WELL Building Standard™ (WELL) envisions this reality and opens this critical dialogue. It provides a roadmap and a comprehensive set of strategies for achieving building and communities that advance human health.

WELL consists of a comprehensive set of features across seven concepts (Air, Water, Light, Nourishment, Fitness, Comfort and Mind). Together, these components address the various individual needs of the people inside buildings, while also setting forth a common foundation for measuring wellness in buildings as a whole. The standard was developed by integrating scientific research and literature on environmental health, behavioral factors, health outcomes and demographic risk factors that affect health; with leading practices in building design and management. WELL also references existing standards and best practice guidelines set by governmental and professional organizations, where available, in order to clarify and harmonize existing thresholds and requirements.

The result is the premier building standard for advancing human health and wellness – and a blueprint for creating better buildings that can enhance productivity, health and happiness for people everywhere.

How to Use this WELLography™

WELLographies™ present research relevant to health and well-being in buildings and communities. The sources included span health, wellness, and scientific and professional literature specific to the seven concepts within WELL, and other core focus areas. WELLographies are meant to complement the WELL Building Standard™ (available at and provide architects, building managers, engineers, and interior designers, among others, with health- and science-focused background to support and guide their efforts to advance the healthy buildings movement.

WELLographies have three primary goals:

  1. Provide background information for key topics relevant to understanding human health as it relates to the built environment.
  2. Synthesize and present the science that underpins the WELL Building Standard™.
  3. Outline specific, evidence-based strategies that building professionals can apply to create spaces that promote health and well-being in buildings and communities.

There are nine WELLographies:

  1. Air
  2. Water
  3. Nourishment
  4. Light
  5. Fitness
  6. Thermal Comfort
  7. Acoustics
  8. Materials
  9. Mind

The Materials WELLography™ has the following sections:

Materials and the Built Environment, which broadly describes how building materials and practices relate to the human experience in buildings.

Material Toxicity and the Human Body, which provides an explanation of the biological mechanisms relating to absorption and processing of toxins and potential impact on these physiological processes due to toxin exposures.

Elements of Materials, which describes environmental conditions or behaviors that are linked to health, focus, or occupant comfort, and that are subject to interventions in building design or policy. Each element includes coverage of associated health effects as well as solutions, interventions that can be implemented to impact the element. Some solutions may address several different elements.

Explanations of Solutions, which provides a definition and/or more detail for each solution.


The chemical industry is central to the global economy, responsible for converting raw materials such as oil, natural gas, air, water, metals, and minerals into more than 70,000 different chemical substances and materials that make up our world.1

Over the past 150 years, the industry has had numerous positive impacts on life expectancy, living conditions, and health around the world. As global population and the demand for manufactured goods continue to increase, the rate of chemical production follows suit. Currently, the rate of chemical production is on the rise at a rate three times greater than global population growth.2 This growth will distribute globally both the benefits and consequences of chemical manufacture, calling for the prioritization and responsibility of advancing safer chemicals and sustainable materials.

The construction industry, which is reliant on the chemical and material industries, is one of the largest and most active sectors globally. When we talk about building materials, we are talking about materials derived from a variety of sources, including both natural and synthetic ones. These materials impart many positive and necessary qualities to a building, but they each have tradeoffs over their life cycle and during their use phase can compromise various important indoor environmental parameters. Chemicals used in furniture, furnishings, paints, and various adhesives and coatings can leach, off-gas, end up in indoor air and dust and in our bodies. One of the most authoritative listings of biomonitoring data for the United States is provided by the Centers for Disease Control and Prevention (CDC). During survey periods (1999-2012) researchers collected blood, serum, and urine from a representative sample of about 2,500 Americans.3 In 2009, the CDC published a report revealing a list of 219 chemicals found in the samples and by 2015 updates presented an additional 46 chemicals identified in their samples.3 Some of these chemicals, such as DDT (dichlorodiphenyltrichloroethane) and PCBs (polychlorinated biphenyls), have been banned for more than 30 years.3 Even more worrisome, these reports from the CDC conclude that many known toxic chemicals can be found in samples provided by pregnant women, findings which are supported by other independent studies.3 This is particularly troublesome since embryonic, fetal and infant development are especially susceptible to environmental toxicants.4 Although individual, synergistic and cumulative effects of chemicals are still poorly understood, in particular for low dose exposures, scientists have established that exposure to toxic chemicals, especially in utero, can increase the incidence of negative health effects.4

Despite gaps in our knowledge regarding the safety of material ingredients used in building products, existing databases and guidelines can provide direction in understanding the tradeoffs in materials and products over their life cycle. Carefully evaluating and selecting building materials and products can be an effective first step to identifying safer materials across installation, use, maintenance, and disposal. In the long run, careful selection of building materials and products can help to promote supply chain transparency and push towards innovation in green chemistry.

The chemicals used in building materials are not constrained to the products they make up.

Figure 1: Raw material resources, use, and fate of building materials.5
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Limited Chemical Disclosure and Hazard Classification

Chemicals are an integral part of all industrial processes and consumer products. As illustrated in Figure 1, the fate of chemicals through their life cycle—from resource acquisition, production/use, and disposal, to subsequent emissions—is complex and multi-layered. The sheer quantity and variety of chemicals flowing through the global economy make the task of evaluating, tracking, and tracing chemicals’ potential health and environmental impacts both critical and extremely difficult.

In 1976, soon after the Environmental Protection Agency (EPA) was established (1970), the U.S. Congress passed the Toxic Substances Control Act (TSCA), the first legislation to regulate new and existing chemicals in the United States.6 TSCA provides the legal framework for managing industrial chemicals used in manufacture. The act was established to support the EPA’s regulation of the production and use of chemicals. At the time TSCA was passed, there were already about 62,000 industrial chemicals on the market. An additional 23,000 chemicals have been added to the inventory since it was established in 1979 bringing the total to 85,000 with 500 to 1,500 new chemicals introduced each year.7 8 9 Of the total number of substances in the inventory, about 7,500 chemicals were produced in annual quantities of 25,000 pounds or more in 2008, while about 2,750 chemicals were high production volume (HPV) chemicals, i.e. produced in excess of 1 million pounds annually.6 Despite the large number of chemicals that have entered the market since, “existing” chemicals make up nearly all chemicals used in U.S. commerce today, comprising about 92% of HPV chemicals. To put this in perspective, only 8% of market chemicals have reached HPV status since 1979, when the 62,000 “existing” chemicals were grandfathered in.10

Figure 2: Percentage of chemicals tested from total market chemicals in the United States.6 7
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Although there have been amendments made to the regulatory framework since the Frank R. Lautenberg Chemical Safety Act was signed into law in 2016, it’s important to provide historical context on how the EPA managed chemicals to date. Authority extended to the EPA for chemical regulation depended on whether the chemical in question was new or existing.11 This comprised three separate but interrelated programs: one for new chemicals entering the market.

New Chemicals

The first program through which the EPA manages chemicals, the New Chemicals Program, requires companies planning to manufacture or import a new chemical to submit a Premanufacture Notice (PMN) to the EPA at least 90 days prior to manufacture or import. New chemicals are exempt from the PMN process if they are manufactured or imported in quantities less than approximately 22,000 pounds per year or have low potential for environmental release or human exposure.12 Hazards reporting was required, however, failure to report a hazard was not penalized creating a disincentive for manufacturers to collect meaningful data. An EPA assessment found that 85% of PMNs lacked data on health effects and 67% lacked health or environmental data.2 Although the EPA may require manufacturers to submit information or conduct toxicity testing as part of the PMN process, the PMN process itself did not necessitate it. Due to the volume of PMNs to process, time constraints and lack of adequate data, most chemicals did not undergo full evaluation. About 80% of PMNs underwent only 15-19 days of assessments, out of a possible 90 days, before they were permitted to go to market. Between 1996 and 2008, less than 10% of chemicals that entered the PMN review process have been regulated in any way, and only 5% have been withdrawn from the review process.7

Existing Chemicals

The EPA employed two programs to manage existing chemicals; the applicable program depended on the chemical’s annual production volume. The first program, The High Production Volume (HPV) Challenge Program announced in 1998, addressed chemicals that were produced in quantities of over one million pounds per year.13 In an effort to narrow the toxicity information gap, the EPA challenged companies that produced these chemicals to “sponsor” them by performing certain voluntary tests and disclosing health and environmental impacts.2 13 In cases where companies did not voluntarily sponsor their HPV chemicals, the EPA took regulatory action under TSCA to have those chemicals tested.13 The incentives to manufacturers participating in the voluntary program, as opposed to imposed regulatory rule, included a degree of testing flexibility and reporting.13 Unfortunately, the effort now discontinued produced limited, incomplete and poor quality data.2 The second program, the Chemical Assessment and Management Program (ChAMP), formerly regulated chemicals produced in volumes between 25,000 and 1,000,000 pounds per year.14 However, the EPA suspended this program in 2009 and replaced it with the TSCA Existing Chemicals Strategy and Work Plan, which has since been superseded by the Frank R. Lautenberg Chemical Safety Act.15 16

Frank R. Lautenberg Chemical Safety Act

Core provisions of TSCA, which had not been updated since the initial adoption in 1976, were revised in June 2016, when the Frank R. Lautenberg Chemical Safety for the 21st Century Act was signed into law.17 Previously, the EPA could impose regulation on the production or use of a new chemical if it could show that there is insufficient data to evaluate the chemical’s health and environmental effects and thus the chemical’s likelihood to pose “unreasonable risk” to “human health or the environment.” In addition, the EPA could impose regulation on the production or use of a new chemical if “the chemical is or will be produced in substantial quantities and either enters or may reasonably be anticipated to enter the environment in substantial quantities, or there is or may be significant or substantial human exposure to the substance.” Protocol for existing chemicals was similar; the EPA was tasked to provide evidence that an existing chemical can or will pose “unreasonable risk” prior to implementing regulatory action.11

The current bill allows the EPA to evaluate the safety of chemicals known to pose a risk through an administrative order as opposed to the previous method of formal rule making, a lengthy legal administrative process that could take years. It also renews the EPA’s authority to evaluate the safety of a chemical prior to market entry by requiring manufacturers to present a safety finding prior market entry and also limits manufacturers’ claim to claiming ingredient contents as confidential. Most significantly, the bill allows the EPA to govern chemicals already on the market, and further, mandates a distinction between the determination of chemical risk, i.e., whether a chemical presents an unreasonable risk, from the decision on how to manage such risk, including costs, benefits, and alternatives. This stands in contrast to previous decades where the EPA was required to analyze the cost and benefit of any proposed regulatory action and prove it was the least burdensome path before concluding that a chemical presented an unreasonable risk. Another major change to TSCA through the Lautenberg the act requires special attention to vulnerable populations, the EPA must consider, assess and eliminate any unreasonable risk a chemical may present to “potentially exposed or susceptible subpopulations.” Though the new bill reflects positive and much-needed adjustments to the past regulatory framework, it is premature yet to speculate on the impact of such a newly updated program.17

Figure 3: Average Fate of New Chemical PMNs Submitted to EPA.18
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Similar to the EPA, which is tasked with administering the federal chemicals management program in the United States, the European Chemicals Agency (ECHA) administers the laws governing the production and use of chemicals throughout the European Union (EU) member states.11 In 2007, the EU adopted a new regulation for the Registration, Evaluation, Authorization, and Restriction of Chemicals (REACH), likely one of the most comprehensive chemical-management systems globally. The EU’s REACH is based on the precautionary principle that a chemical must be proven safe before it is put to market use. For example, REACH requires chemical manufacturers to develop and share data, including data about the physical and chemical properties as well as human health and ecotoxic effects of chemicals produced above certain volumes. REACH also provides regulators the authority to require manufacturers to submit testing or other data necessary for further chemical evaluation without first having to provide evidence of risk. In fact, a chemical identified as a Substance of Very High Concern (SVHC) based on potential serious human and environmental impacts, must abide by specified labeling requirements and communication of content and use throughout the supply chain. Further, those SVHCs on the authorization list (Annex XIV) are restricted and may not be produced or used without special authorization and a demonstrated need or benefit of use.11

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Figure 4: Trends in breast milk contamination (PBDE, DDT and PCB) in Sweden.20
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A sound chemical regulatory framework is critical to protecting human health from undue chemical hazards exposure while preserving the benefits of chemical sciences. Long-term, large-scale studies such as the CDC’s National Report on Human Exposure to Environmental Chemicals have not only identified chemicals of widespread concern but more importantly, have documented policy change impacts on human exposure.21 For example, DDT, a well-known commercial organochlorine insecticide used widely in agriculture, is known both to endure in the environment without degrading and to bioaccumulate in animal tissue. Because DDT and its residues are drawn to fat, measures of these organochlorines in human breast milk are often six to seven times higher than in blood. Although DDT and its residues have been measured in more than 60 countries, only a handful of nations have comprehensive data using large study populations over time. In Sweden, long-term testing of human breast milk for the presence of DDT and DDT residues has shown a substantial decrease in the organochlorine in response to the country’s 1970 restriction of the chemical and subsequent ban in 1975.22 Similarly, a gradual and consistent decline is evident for PCB concentrations, potentially due to continued concern over the pollutant and efforts to move away from its use by European Union states. In contrast to DDT and PCBs, concentrations of the flame retardant PBDE demonstrate exponential increase, consistent with decades of increased use (see Figure 4).23

Despite the fact that industrial processes around the world are often known to leave unintentional, toxic residues in end-material products, disclosure of content or ingredient data for end materials and products is greatly lacking. This information is not only important for chemicals that go into extended- use products—where an estimated 95% of chemicals largely used in construction lack sufficient data on human health effects24 — but is also critical to manufacturing and disposal steps. In the United States, in addition to gaps in product information, the regulatory approach to date has allowed substitutions to many banned products to re-emerge on the market. These substitutions, although slightly altered in chemical structure, often carry similar or possibly worse health and environmental risks.25 For example, following the EPA ban of PCBs in the late 1970s a secondary class of flame resistant products emerged on the market, PBDEs.26 While structurally similar, they were deemed a separate class of compounds from PCBs, and their use increased steadily over the course of PCB phase-out and elimination. This “regrettable substitution” trend is not unique to this pair of compounds and continues to threaten intentions to limit the use of hazardous chemicals. Despite initiatives lead by the EPA such as Green Chemistry, the regulatory environment to date has hampered the EPA’s ability to shift towards more positive and safer materials that have reduced health and environmental risks. While Green Chemistry initiatives promote the manufacture of safer chemicals, it doesn’t necessarily protect the market from the re-emergence of harmful substitutes.

Disclosure of content or ingredient data for end materials and products is greatly lacking.

Materials and the Built Environment

The focus of construction materials has shifted over the past decades from a question of durability and mechanical effectiveness to sustainability and potential impact on human health. Building materials can be a source of, and contribute to, indoor air pollution.

Thousands of different chemicals are present in building materials, many of which may be benign.

Because we spend up to 90% of our time indoors, such materials can have a significant impact on our health and well-being.27 This is increasingly important because recent energy conservation models promote tightly sealed buildings that minimize infiltration of outdoor air. These new models lead to an increase in the concentration of indoor air contaminants that may accumulate from building materials or other sources within or outside the structure. Further, building materials are intended for long-term use, extending potential exposure to their chemical constituents for many years to come. Given these considerations, the selection and evaluation of building materials is a chief factor in avoiding or mitigating poor indoor air quality and promoting health and well-being within the built environment.

However, some chemicals in building materials are not innocuous, including some that are known toxicants including but not limited to:28

  1. Asbestos, found in insulation, pipe covers, and various other applications in older construction;
  2. Certain unreacted diisocyanates that may be found in polyurethane products like upholstery as well as certain types of commercial paints;
  3. Certain phthalates, found in plasticizers used in PVC and other plastics;
  4. Toxic metals, including lead, that have been used in wire insulation, solder, dyes, and pigments, and may be present in older construction;
  5. VOCs, found in some paint, adhesives, insulation, and carpet, among other products
  6. Flame retardants such as PBDEs;
  7. Urea Formaldehyde used in particleboard, plywood, or fiberboard;
  8. Chromated Copper Arsenic (CCA) used as an anti-rot treatment for wood.

There are tens of thousands of chemicals used in building products for reasons of cost, performance, physical safety, and the like. While some portion of these chemicals can be safe in their original state, others can be hazardous. While the list above is not exhaustive, it is intended to highlight some of the most well-tested substances for which hazards and human health endpoints have been established. Due to the already substantive list of existing chemicals currently used and the emergence of countless novel products each year, it is challenging to compile and maintain a complete record of chemicals of concern. To help shift the industry towards green chemistry, there is a need for a comprehensive approach to assessing and selecting building products. While this WELLography is not meant to bridge this gap, it does aim to create awareness and provide education on the implications of some select hazardous chemicals found in building materials.

Material Toxicity and the Human Body

To understand the importance of hazard and exposure reduction in the built environment, it is important to understand the nature of toxicity and how a hazardous substance can impact the human body.

The toxicity of a chemical—the extent to which it can do damage to the body—depends on a number of factors including the route of exposure, the dose and its duration, the physical form of the exposure, and the substance’s specific chemical form. In addition, some human variables can affect toxicity, such as an individual’s age at the time of exposure, genetics, pregnancy, or compromised health, and numerous behavioral influences, such as the presence of additional risk factors, for example smoking history. It is important to note that “the presence of a chemical does not imply disease.”29


The route and level of exposure depend on properties of the chemical in question and the medium of transference—in the context of the built environment, the medium is typically air, water, and surfaces (see Figure 5). Building materials may emit volatile organic compounds (VOCs) (such as formaldehyde) in gaseous form, or they may contribute toxic compounds or elements (such as lead) to indoor dust as materials disintegrate or wear down. Building materials may also act as a sink, adsorbing gaseous chemicals and various VOCs from the environment and releasing them over time.

Figure 5: Route of entry and exposure medium of toxicants into the human body.30
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Inhalation of airborne substances, gaseous chemicals, vapors, and dust or mists are common routes of indoor chemical exposure.31 When inhaled, airborne chemicals enter the respiratory tract and pass into the airways and lungs. The depth to which a substance travels depends on its phase (gaseous, liquid, or solid), particle size (for solids and liquids), shape and physical properties (density). Water solubility or electrical charge of certain compounds may also play a role in how reactive a chemical is when inhaled. If deposited within the upper respiratory system, the effect is likely irritation or perhaps allergic reaction. If a substance is able to travel farther into the lungs, it can damage the lung tissue (as in the case of asbestos) or be absorbed into the bloodstream.31 Once in the bloodstream, substances can circulate throughout the body and affect various tissues, organs, and systems. Vapors and ultrafine particles (less than 2.5 µm in diameter) can typically be absorbed into the bloodstream.32

Skin Contact

Dermal exposure can be expressed as a product of contact and absorption. Various factors of both the contact surface (skin) and substance implicate the amount that is able to enter the body and interact with biological processes. Conditions of the skin barrier such as integrity, location of contact, and the surface area exposed dictate how readily a toxin is able to pass through the skin barrier. Physical and chemical properties of the compound itself, such as particle size, presence of inorganic or organic components, and hydrophobicity, also affect the degree of absorption.33 34 The amount of contaminant absorbed determines the amount that is ultimately able to reach target organs.35 As with inhaled substances, chemicals that enter the bloodstream via the skin can affect various tissues, organs, and systems. Chemicals not systemically absorbed may instead cause local toxicity in the form of superficial skin irritation or sensitization. Examples of building materials that may cause adverse dermal effects include partially cured polyurethane coatings or methacrylate adhesives. Depending on the degree of toxicity and duration of contact, effects can range from mild discomfort to permanent skin damage.36 37


Exposure via ingestion occurs through the digestive tract. Once a chemical is ingested and enters the digestive tract, its bioavailability, or the degree to which the chemical can be absorbed into the body, affects further exposure.35 38 Bioavailability is influenced, in part, by the chemical’s physical form and solubility, such as hydrophobicity. Hydrophobicity describes the polarity of water molecules and their tendency to repel other non-polar molecules and is commonly quantified for toxins using octanol, an organic solvent, which is widely used as an indicator for bioavailability.39 Chemicals used in building materials can leach or volatilize over time and contaminate water or food to be ingested by inhabitants.38 Additionally, physical abrasions to materials in the built environment from general use, wear-and-tear, can result in exposure to smaller particles of a substance, which can be directly ingested or inhaled, or contaminate food or water supplies.

Because some chemical compounds may be found in household dust, young children—who crawl or spend time on the floor and frequently put their hands or other objects in their mouths—are more likely to ingest contaminants. Contact with substances for which ingestion is the primary route of exposure is greater for small children given their increased hand-to-mouth activity and large air, food, and water intake in proportion to their body weight compared to adults.40 41 Further, health effects may be more serious in children, as children are particularly susceptible to adverse health effects during developmental years.4


Once a chemical enters the body, it may target parts of the body far from the initial exposure site, triggering toxic effects through interaction with cells, tissues, and organs (Figure 6).36

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Toxicity Characteristics

Toxicology deals with characterizing potential adverse effects posed by chemical or biological substances in cells/tissues. It uses a variety of in vivo (living) experimental techniques in both animal and human models (for certain endpoints such as dermal toxicity) and in vitro (i.e., in glass) and in silico (i.e., digital) models to determine the relationship between dose and response.

An accepted precept in toxicology is that the dose of a chemical or substance determines its effect and to some extent the degree of its effect, so any evaluation of toxicity requires an assessment of dose. Central to the dose-effect relationship is the assumption that there is a dose below which no detectable response occurs.43 However, there are substances whose toxicity profile does not abide by these rules. There are doses at which certain substances, of otherwise low or moderate toxicity, have no adverse effect but that nonetheless persist or accumulate in the environment or organism. Chronic doses of these substances may cause serious damage to an organism. For these reasons, there are also some substances, such as lead, for which there are no safe levels.44 45 46 In addition, some substances, for example, certain endocrine disruptors do not follow the traditional dose-response curve, and have been shown to have negative health effects at low dose that are not predicted by effects at higher doses.47


Persistence describes a chemical’s tendency to resist degradation by chemical, physical, or biological mechanisms. The more persistent a hazardous chemical is, the greater the chance that an organism will come in contact with it and that levels of the chemical will increase in the environment (thus increasing its danger).

A chemical’s half-life, used as a measure of persistence, signifies the amount of time required for half of a substance to degrade or break down. Persistence is often measured in the field. If the compound is able to survive long enough for it to be either transported over long distances and/or be available for uptake by organisms, it is considered to be persistent. Chemicals that persist in the environment have a high potential for accumulation and uptake by living organisms, thereby increasing the chances for bioaccumulation within an organism and within the food chain.48 The United Nations Economic Commission for Europe’s Convention on Long-Range Transboundary Air Pollution (LRTAP) uses a half-life in air of more than two days as a screening criterion for identifying Persistant Organic Pollutants (POPs), and half-lives in soil, water or sediments of two to six months.49

Signatory nations of the Stockholm Convention on Persistent Organic Pollutants of 2001 and subsequent treaty of 2004 have agreed to reduce or eliminate the production, use and/or release of the 12 POP chemicals known as the “Dirty Dozen.” Subsequent meetings adopted amendments to the list, finalizing 27 chemicals.50 Although it’s not possible to determine with certainty whether which POPs in Table 1 are found in or associated with building materials, some have well-known uses. In the past PCBs have been used in electrical insulators, transformers and capacitors, and as plasticizers and sealing materials for expansion joints, among other uses.51 Although most developed nations have taken action to ban or restrict certain POPs, a large number of developing nations are working to restrict production, use, and release of POPs. Further, existing materials containing POPs require environmentally sound elimination. Reports from the Stockholm Convention, which requests Parties to report on progress in eliminating PCBs every five years, indicates that progress varies significantly across UN regions and that a large number of countries are not on track to achieve environmentally sound elimination of PCBs by 2028.52


Chemicals can accumulate in the body if not readily eliminated. The rate of accumulation depends on the fat content of the organism and rates of uptake, elimination, and metabolic transformation. As a general rule, the less water-soluble a substance (and therefore more fat-soluble), the more likely it is to accumulate within an organism. The bioaccumulation of a substance is correlated to the substance’s octanol-water partition coefficient (KOW). This coefficient measures how hydrophilic (“water-loving”) or phobic (“water-fearing”) a chemical is using octanol as a surrogate for lipids. This means that increasing hydrophobicity (or in other words, lipophilicity) leads to an increasing tendency for bioaccumulation.53 Bioaccumulation not only drives the concentration of some toxicants in the food chain, but it also contributes to increased body burdens of these compounds and determines the concentration of such compounds in breast milk.54

Persistent bioaccumulative toxicants (PBTs) have garnered international concern because of their inherent hazard combined with their tendency to resist degradation and accumulate in food chains.55 PBTs include some of the most potent carcinogens, mutagens, and reproductive toxicants, such as mercury and DDT. Biomagnification, the consequence of bioaccumulation, describes processes that lead to higher concentrations of a contaminant in a given organism based on the hierarchy within the food chain. Organisms higher up in the food chain have higher concentrations of a contaminant as it passes through trophic levels.56

Toxicity Endpoints

A toxicant’s health effects can be transient, persistent, cumulative, local (at the sight of initial contact) or systemic, and cause either morbidity (illness) or mortality (death). A chemical agent’s ability to do harm depends on the extent to which the chemical can be absorbed by the body, its chemical structure (which determines chemical activity), and the body’s ability to metabolize or eliminate it. An exposure-response to toxic chemical agents can be acute or chronic and may vary depending on the individual’s site of exposure, age, genetics, gender, diet or health status, among other factors.43 In addition to endpoints at the individual level, it is also important to consider toxic environmental endpoints, which are often indirectly associated with human health outcomes. For example, factors that contribute to the accumulation of toxicants in water supplies or soil have implications for human health as these toxins can advance up the food chain and accumulate in human tissue. Further, toxicants that affect certain species, such as bees, also pose substantial risks to the human food supply, which subsequently threatens food security and human health.

Figure 7: Exposure and fate of toxicants.43
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Carcinogens are chemical substances or mixtures that are “capable of increasing the incidence of malignant neoplasms, reducing their latency, or increasing their severity or multiplicity”.57 Some carcinogens do not affect DNA directly but may lead to cancer through increased cell division, thereby raising the chances of DNA mutation. Further, carcinogens do not always cause cancer, but “have different levels of cancer-causing potential”.58 Factors that influence the potential development of cancer include type, length and intensity of exposure as well as the individual’s genetic makeup.58


Genotoxicity pertains to a toxicant’s ability to interact with DNA and/or non-DNA systems leading to damages in the genetic information and causing alterations in genetic material.59 The alterations can have both direct and indirect effects on DNA: mutations, unscheduled DNA activation, and direct DNA damage. A genotoxicant may cause a lesion in DNA that results in cell death or mutation. Therefore, although all mutagens are genotoxic, not all genotoxicants are mutagens, as they may not cause retained alterations in DNA sequence.59


A mutagen refers to a substance that can instigate changes in the DNA of a cell or the “induction of permanent transmissible changes in the structure of the genetic material of cells or organisms” typically “involving a single gene or a block of genes”.60 Chemical mutagens alter the delicate chemistry of base pairs (nucleotides) that make up the DNA chain through a variety of mechanisms. Some mutagens strip DNA nucleotides of essential functional groups so that the nucleotides resemble different base pairs. Subsequent DNA replication permanently incorporates these changes. Other mutagens can look similar to existing nucleotides leading to insertion or deletion of an extra base pair during DNA replication.61


Teratogens are substances that can disrupt elements necessary for normal development or growth resulting in birth defects or abnormalities at later developmental stages such as growth retardation, delayed mental development or other congenital disorders that may not include structural malformations.62 Approximately 3 to 5% of American children are born with developmental defects, and of these, 2 to 3% are considered to have “teratogen-induced malformations,” meaning the malformations are a result of environmental exposures during pregnancy or induced by medical treatment.63

Endocrine Disruption

The endocrine system keeps the body in balance, maintaining homeostasis and guiding proper growth and development. Endocrine disrupting chemicals (EDCs) are agents that can disrupt the body’s endocrine system and produce adverse “developmental, reproductive, neural, and immune” effects.64 Once absorbed into the body, an EDC may alter hormone levels or mimic hormones in the body, such as estrogens (female sex hormones), androgens (male sex hormones), and thyroid hormones. Lastly, an EDC can alter the natural production of hormones—for example, by blocking the body’s hormones from binding and preventing necessary cellular signals from taking place.64 EDCs can have effects at low doses that are not predicted by effects at higher doses, challenging the traditional understanding of dose and effect.

Figure 8: Cellular response mechanisms to three major types of endocrine disruptors.64
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Neurotoxicants target the nervous system and disrupt neuron signaling through alteration of its structure or function and include naturally occurring and synthetic compounds, for example, compounds such as Botulin (produced by Clostridium botulinum bacteria) and PBDEs (widely used flame retardants).65 Neurotoxicants’ effects can include dizziness, confusion, nausea, and vertigo and even long-lasting effects (e.g., dementia).66

The developing human brain is especially susceptible to neurotoxic exposure. Low-level exposures that would have no adverse effect on an adult can have negative impacts in-utero or during early childhood and can manifest as functional impairments or disease at any point in life, from infancy to old age.67

Figure 9: Early life exposure to neurotoxic chemicals and adverse effects.67
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Reproductive Toxicity

Reproductive toxicants, or reprotoxicants, are substances that can have adverse health effects at various stages of human reproduction and development. Damage can manifest during the development stage of offspring or lactation, or affect adult sexual function and fertility.68 This includes any toxicant that interferes with normal development, before or after birth, due to parental exposure, exposure in utero, or post-natal exposure up to the time of sexual development.69

Developmental Toxicity

Developmental toxicants are compounds that affect the developing offspring from pre- or post-natal development, and through sexual maturation. Major effects of developmental toxicity include “1 death of the developing organism,2 structural abnormality,3 altered growth, and4 functional deficiency”.70 There is an overlap with regards to the effects of developmental toxicants with that of reproductive toxicants. Depending on the classification framework, developmental and reproductive toxicants are sometimes defined together but otherwise classified differently. For example, The Globally Harmonized System of Classification and Labeling of Chemicals (GHS), consistent with most frameworks with the exception of EPA’s Design for the Environment’s (DfE’s) Alternatives Assessment Criteria for Hazard Evaluation, incorporates developmental toxicity in the definition of reproductive toxicity, but otherwise classifies them separately.71

Elements of Materials

The life cycle of an industrial or commercial product includes the principal stages of manufacture and use: extraction, production, construction and maintenance, occupancy and demolition, and disposal.

The United States consumes about 25% of global raw resources, a large majority of which (60%) is consumed in the building industry.72 The extraction of raw material, which includes the identification, means of extraction and transporting of the raw material can result in environmental releases of contaminants, and worker exposure to potentially hazardous materials. Natural or anthropogenic contaminants from mined ores can also contribute to toxic residues in end-material products.73 Following extraction, exposure hazards are associated with production, construction, and demolition, including exposure to dust, fumes, solvents, and gases during maintenance, where workers may be exposed to hazardous chemicals in the absence of the exposure and ventilation controls required in production or construction settings. The people most at risk are involved in indoor work, where exposure to potential hazards is concentrated and confined, such as finish, maintenance, and renovation work. Assessing hazards for building inhabitants is less acute since day-to-day use should not involve significant exposure to fumes, solvents, gases, or hazardous dust. However, the ongoing exposure to chemicals from building materials can be chronic and rarely limited to a definitive group of chemicals or route of exposure, making consideration of potential health impacts difficult to assess.

Figure 10: Potential Chemical Hazards In The Production, Use, And Disposal Phases Of A Building Material Or Product Life Cycle.
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Each Element below describes a particular building material or related chemicals, how it affects the human body, and best practices for reducing exposure or potential harm from that material. The Elements reviewed are those most commonly used and potentially harmful chemical ingredient contents in building materials.

  1. Asbestos
  2. Toxic Metals
  3. Volatile and Semi-Volatile Organics
  4. Halogenated Flame Retardants
  5. Polychlorinated biphenyls (PCBs)
  6. Bisphenol A
  7. Alkylphenols (APs)
  8. Perfluorinated Compounds
  9. Organochlorinated Compounds
  10. Polyurethanes
  11. Wood Preservatives
  12. Refuse Derived Fuels

Mineral Fiber Based Materials

“Mineral fiber” is used to describe elongate mineral particles (EMPs), such as asbestos (“asbestiform” fibers) and needle-like or prismatic crystals (“non-asbestiform” fibers). EMPs come from extraction, breaking up, or “fracturing” of non-fibrous minerals.74 There is debate as to whether non-asbestos mineral fibers have substantial hazards. Asbestos is a well-known and serious health hazard. Dangers associated with the production, use and demolition or disposal of asbestos is the focus of the following text.

1. Asbestos

Asbestos is the common name applied to six fibrous minerals that belong to the serpentine and amphibole mineral families.75 With properties that make it resistant to high heat, fire, electrical damage, and chemical damage, it has been used in products ranging from brake linings and electrical insulation to building materials and fireproofing. Asbestos fiber characteristics, length, and strength, tend to determine use. Longer fibers are used in textiles and electrical insulation, while medium-length fibers are ideal for use in cement pipes and sheets, friction materials, and gaskets. Short fibers work best to reinforce plastics, floor tiles, and roofing felts. Current use of asbestos varies globally, while some countries have banned its use, others impose strict regulations on manufacture and use, while others apply minimal intervention.75

At one point, thousands of products containing asbestos were on the market. However, asbestos was subsequently identified as a fibrogenic product to the lung (i.e., development of asbestosis) and a significant carcinogen contributing to mesothelioma and other forms of lung cancer.75 Current use of asbestos greatly varies across countries, while some have strictly regulated the material others have minimally intervened. In 2007 world production of asbestos reached 2.20 million metric tons, increased from 2.18 million metric tons in 2006. Many building materials in existing structures contain asbestos, and it is still used in the manufacture of some select building products. For example, roofing materials products, including coatings and compounds, accounted for over 80% of asbestos used in the United States between 2006-2007.75

Figure 11: asbestos use in building materials.76 77
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There are two main types of asbestos—serpentine and amphibole—classified by the shape of the mineral fibers.78 The mineral chrysotile, owing to its flexibility and ability to be spun into fibers, is the most commonly used form of asbestos. It is comprised of fairly long and flexible fibers capable of being entwined and woven, which are characteristic of serpentine asbestos. Amphibole asbestos, which includes the minerals amosite, anthophyllite, crocidolite, tremolite and actinolite, is made of fibers that are less flexible and more brittle than serpentine asbestos and therefore less suitable for manufacturing purposes. Regulations on asbestos apply to all six minerals.78

Vermiculite, another material used in similar applications, such as insulation, remains a point of controversy in the field due to a history of asbestos contamination. Vermiculite extracted in the past from mines in Libby, Montana, was contaminated with asbestos; that mine was the source of 70% of vermiculite mined in the U.S. between 1919 and 1990.79 The EPA advises that vermiculite insulation from Libby should be considered and treated as if it contained asbestos.80

The U.S. Department of Health and Human Services, the EPA and the International Agency for Research on Cancer have classified asbestos as a known human carcinogen. However, despite well-known health hazards, some areas of the world still produce and utilize asbestos. Only 57 countries have enacted bans or restrictions on asbestos production or use.78 Although asbestos use is regulated in the United States,81 82 it is not banned. In 1989, after nearly a decade building its case, the EPA issued the Asbestos Ban and Phase-Out Rule under TSCA.83 Challenged by manufacturers, the U.S. Court of Appeals struck down most of the rule in 1991 citing lack of substantial evidence to justify the ban and clearing the way for various products to legally contain trace amounts of asbestos. The portion of the rule that did survive the appeals process mandates, under TSCA, that in addition to the new use products ban, i.e., the use of asbestos in products that have not in the past contained asbestos, the manufacture, import, processing, and distribution of corrugated paper, roll board, commercial paper, specialty paper, and flooring felt is banned.84 The production and use of asbestos are also regulated under the Clean Air Act and the National Emission Standards for Hazardous Air Pollutants (NESHAP).

All types of asbestos can become airborne and inhaled. The small size of the fibers allows them to be respired, that is, they can enter the respiratory system and reach the lungs when inhaled. Factors known to determine the pathogenic effect a fibrous material will have on the body include fiber size (diameter and length), durability or persistence in the lung,78 85 and shape. Long, thin fibers travel deeper into the lungs, reaching the lower airways and lungs where they can be retained, making them more toxic than short, wide fibers which tend to be deposited in the upper respiratory tract and can be cleared but still play a role in the pathogenesis of asbestos exposure.86 Amphibole asbestos may be more toxic than chrysotile due to a difference in physical properties; while chrysotile tends to break down in the lungs and is cleared, amphibole is persistent and can build to high levels in lung tissue.87

Although the use of asbestos dates back more than 2,000 years, its industrial manufacture was not fully established until the mid-1800s, and it was not until the early 20th century that lung diseases and deaths associated with the manufacturing of the material became evident. By the early 1970s, significant health concerns lead to regulations on asbestos products under the Clean Air Act, coinciding with the peak of its use. In 1980, a National Institute of Occupational Safety and Health (NIOSH) and Occupational Safety and Health Administration (OSHA) committee work group determined there was no safe level of exposure to asbestos and recommended an occupational Permissible Exposure Limit (PEL) based on the lowest measurable airborne level (0.01 fibers/cc), also the clearance level required for asbestos abatement.88 According to the World Health Organization, asbestos is still currently one of the most significant workplace carcinogens, making up about half of deaths associated with occupational cancer.89 Besides health impacts associated with manufacturing, which is typically no longer an issue in most developed nations, asbestos is a global waste disposal concern, including in the United States. Though the handling and disposal of friable (able to crumble) asbestos waste is regulated, the EPA estimates asbestos emissions from all waste disposal sites to be about 499,000 pounds (22.7 metric tons) per year, and estimates this figure could be reduced to 1,320 pounds (600 kilograms) per year if sources are in full compliance with NESHAP. Unfortunately, data for exposure from asbestos disposal sites, quantity disposed, of location, and status is generally lacking.90

Many buildings throughout the world were constructed with asbestos-containing materials (ACM). Insulation, dry wall, and ceiling and floor tiles used within the built environment can frequently contain asbestos and consequently release fibers into the air due to disturbance or wear and tear. Although indoor levels of asbestos may be 10 to 100 times higher than outdoor levels, these levels are still 10,000 to 100,000 times lower than those found in most settings where asbestos or ACM are produced.91 Also, measured indoor air values for airborne asbestos vary greatly. This is in part due to the concentration, type, and condition of the ACM. For example, asbestos used in floor tile is less likely to come apart with age and wear than that used in insulation or in spray coating. Further, release of asbestos fibers from ACM can depend on traffic and other human factors that promote friction, wear and tear, and the release of fibers.90 One of the largest and most extensive studies evaluating indoor asbestos concentrations involved the sampling of air in 315 buildings (indoor and outdoor) over a five-year period. In total, 2,892 air samples were obtained from occupied public, commercial, residential, school, and university buildings in the United States.90 Airborne concentrations of particles can only be verified using light microscopy when a length to width ratio of 3:1 or a length of 5 µm. When a particle or fiber has a diameter of 0.25 phase contrast microscopy, one of the most common methods of analysis is not as effective at identifying, and therefore, quantifying asbestos.90 The results demonstrated that indoor concentrations of asbestos, regardless of the condition of ACM, were generally very low. The average concentration of all asbestos was low, at 0.02 structures/ml. There were no asbestos fibers detected in 48% of indoor samples and 75% of outdoor samples.90

While asbestos exposure has been greatly reduced through policy-level limitations on its manufacture and use, individuals who work with building materials, especially in older buildings, are at increased risk of exposure.92 Asbestos-related diseases are still a major health concern. From 1990 to 2010, over 425,000 life years were lost due to asbestos-related diseases.93 As recently as 2014, the WHO maintained their position that there is no such thing as a safe exposure to asbestos, as all known forms of the material are carcinogenic.94 The IARC classifies all forms of asbestos as carcinogenic to humans.95 There is no threshold level set for the carcinogenic risk of asbestos, although, the rate of disease is related to the fiber type, size, dose, and packaging of the asbestos. Activities such as smoking in conjunction with asbestos exposure significantly increase the risk of lung cancer and mesothelioma.96

Health Effects

Respiratory System

Lung damage and asbestosis. Non-cancer effects associated with asbestos exposure include asbestosis, a chronic inflammation of the lungs; scarring; and restricted lung function resulting in shortness of breath. Other asbestos-related pulmonary conditions include pleural, pericardial and diaphragmatic plaques, which involve calcification, and thickening or fluid buildup of the lung lining.87

Endocrine System and Respiratory System

Lung cancer. Asbestos fibers can be released into the air when materials are handled, disturbed, or damaged. Asbestos exposure has been associated with lung cancer through animal and epidemiological studies.95 97

Mesothelioma. Mesothelioma, a cancer of the pleura (the lining around the lungs) and peritoneum (lining around the abdomen), is almost exclusively linked to asbestos exposure.96 Exposure to asbestos and incidence of mesothelioma have also been linked through animal and epidemiological studies.97 98 99


1. Organic Fiber Substitutes

The most effective way to mitigate the risk of asbestos-related disease is to cease its use and promote the use of alternatives.

Organic fiber substitutes offer risk-reduction potential in building materials to both the environment and human health. Organic substitutes including flour-based fillers and cellulose fibers are but a few popular alternatives. Other organic substitutes including various thermoplastics and silica fibers are additional alternatives that also offer other benefits including insulating properties and added strength.100

2. Asbestos Abatement

To prevent exposure to certain materials that pose a risk due to their state, abatement may be necessary. At the federal level, both the EPA and OSHA have published guidelines and regulations for asbestos abatement. While EPA regulations focus on the abatement of ACM, identification of friable asbestos in schools, industrial emission of asbestos fibers, and the disposal of asbestos waste, OSHA focuses on worker protection in occupational settings. Further, a wide variety of asbestos regulations and/or guidelines have been established at the state level. Most states have adopted, matched, or created more stringent rules than those found at the Federal level.91 101 102

Toxic Metals

“Heavy metal” describes a number of naturally occurring elements that have a high atomic weight and density, at minimum five times more than that of water. Heavy metals lead, mercury, arsenic, cadmium, and chromium are known to have negative systemic effects, even at lower doses, and so are a priority concern in terms of public health. Other heavy metals, for example, iron, zinc, and copper, are considered essential nutrients and play important roles in terms of biochemical and physiological function but may cause adverse health effects in excess.103 Most heavy metals can have negative health effects at high doses, and as previously stated, some can have profoundly negative effects at relatively low levels of exposure. Because heavy metals are inherently persistent, often bioaccumulative, and have significant toxic effects, they are a priority concern in terms of human exposure. Many of these heavy metals, like antimony, cadmium, lead, chromium, and mercury, have been or currently are being used in building materials. While some of these materials are more strictly regulated than others, their health effects must be considered when building new projects.104

1. Lead

Lead is a corrosion-resistant, dense, and malleable blue-gray metal. It has been used for much of human history for various building applications. Lead sheets are used as architectural metals in roofing, flashing, gutters and gutter joints, and roof parapets. For many decades, until it was banned in 1977, lead-based paints were commonly used in homes and other buildings. Lead pipes were used for connecting buildings to water mains, a use that declined after 1930. Existing lead in the built environment is an ongoing health issue.105 106

Lead is a potent toxicant that can affect most systems and organs in the body. Young children are particularly vulnerable to lead poisoning, which can result in learning problems, lower IQ, slowed growth, hearing problems, anemia, and other issues. In adults, lead exposure can lead to constipation, nausea, irritability, headache, forgetfulness, and depression.107

Historically, the majority of lead exposure has come through lead paint, which children would ingest, or residents would inhale through exposure to dust. Though it is banned in the United States, lead is still used in various building materials, including roofing shingles, tank linings, and electrical conduits.108

This means that construction workers especially, but also anyone who lives or works in a building that is built with lead-containing construction materials, is at risk of exposure.109 Furthermore, individuals who live or work in older buildings, or perform maintenance or demolition on said buildings, are also at higher risk of exposure.

Because of lead’s known health effects, in 1977 the Federal government restricted the use of lead in the manufacture of paint and paint-based products for residential and public buildings, and for use in toys and furniture.110 In addition, the 1986 Safe Drinking Water Act (SDWA) required the use of lead-free pipes and fittings (containing less than 8% lead) in the construction or repair of public water systems or plumbing used to provide water for human consumption. This ban also applied to the manufacture of solders and flux, which were designated lead-free if containing less than 0.2% lead. Prior to the SDWA lead ban, solders used in water piping commonly contained up to 50% lead.111 In 2011, the U.S. Congress enacted the Reduction of Lead in Drinking Water Act, amending the SDWA so that the maximum amount of “lead-free” plumbing components was reduced from 8% to a weighted average of 0.25%.112 To further control exposure, the EPA has established standards for lead in household dust on floors (40 µg/ft²) and window sills (250 µg/ft²) to identify harmful conditions and to create “clearance levels” to ensure lead abatement work avoids future poisonings.113 In 2008, the EPA also promulgated rules to safeguard against harmful lead exposures during renovation, repair, and painting projects that could potentially “disturb lead-based paint in homes, childcare facilities and pre-schools built prior 1978”.114 Additionally, the EPA requires that firms conducting such renovation be certified and workers trained to avoid creating lead hazards.114

Lead poisoning has been well documented through antiquity, however, it was not until the 20th century that the epidemic of lead poisoning in industrializing nations led to the need for regulatory action. Further, it was not until the latter part of the 20th century that the subclinical effects of lead were recognized. After the 1920s, environmental pollution by leaded gasoline was a serious, alarming public health problem, until restrictions of its use in the mid-1970s resulted in a drop in the mean lead blood values of adults and children from 10-15 mg/100 ml (0.5-.72 mm/l) to much less than half of these values by the early 2000s.115

The CDC uses a reference level of 5 µg/dl and further notes that “even low levels of lead in blood have been shown to affect IQ, ability to pay attention, and academic achievement” and that “effects of lead exposure cannot be corrected”.116 Lead poisoning resulting from occupational exposure (the mining of lead or manufacture of lead-containing products) was first reported in 370 B.C. By the 19th and early 20th centuries it had become a common occupational hazard. Despite improved worker conditions, acute occupational exposure to lead resulting in clinically significant symptoms is still common in developing countries.117

Acute occupational lead exposure is not a significant issue in developed countries. However, there is concern regarding low-level chronic exposures to lead in non-occupational settings, especially among children.118 Exposure to lead among the general population includes multiple pathways (air, water, food, soil) and sources (paint, solder, water pipes). Although sources are bound to differ depending on country, region, and demographics, lead in the atmosphere is a substantial contributor to lead body burden and is the most widely distributed source of lead in the environment. Food and water are also significant sources of lead.118

Chronic exposure to low levels of lead is still a significant public health issue, even in developed countries and especially among certain demographics and disadvantaged groups.117 Studies show that negative health effects from lead exposure in non-occupational settings is due to chronic low-level exposures through household dust (from deteriorated lead-based paint). Nearly 35% of US homes have lead-based paint and about 22% have active lead hazards (e.g., lead dust in excess of EPA standards).119

Health Effects

Cardiovascular System

Blood pressure. Studies examining adults in the general population have found that increased bone and blood lead levels are associated with hypertension (an increase in blood pressure). In occupational workers exposed to lead, as well as adults who had been hospitalized for lead poisoning in childhood, studies have shown a significantly increased mortality rate due to cerebrovascular disease, the most important underlying cause of which is high blood pressure.120

Endocrine System

Although there is no conclusive evidence for carcinogenic effects of lead in humans, animal studies provide sufficient data. The IARC defines inorganic lead as a “probable human carcinogen” but asserts that there is insufficient data to associate organic lead compounds with cancer in humans.121 122

Nervous System

Neurotoxicity. The nervous system is the main target for lead toxicity. Children are especially vulnerable to lead’s neurotoxic effects. The EPA reports that exposure to lead, even at low levels, in early development are associated with negative impacts on intelligence quotient (IQ), learning, memory, and behavior.123 There is no known safe level of lead exposure for children.124 Neurological symptoms of occupational workers (those involved in the production, use, or incorporation of mercury in products) have been observed at blood lead levels of 40 to 120 µg/dL.

Neurobehavioral effects. Neurobehavioral outcomes in children have been studied extensively. Several major prospective cohort studies have used prenatal and postnatal blood lead levels and bone lead levels to associate lead exposure to negative outcomes in IQ, learning, memory, and behavior. To measure neurobehavioral changes, IQ tests, the Mental Developmental Index, and the Weschsler Intelligence Scale for Children, in addition to other testing batteries, were used.120 125

Reproductive System

Reproductive and developmental effects. Several occupational and environmental exposure studies have shown negative reproductive outcomes in both women and men who have been exposed to high levels of lead. Women with higher blood lead levels were shown to have a higher risk of spontaneous miscarriages and pre-term delivery. Elevated blood lead levels in men are associated with alterations in sperm and decreased fertility. Developmental effects have also been noted including low birth weight, altered growth and altered development of the reproductive in offspring exposed to elevated blood lead levels in the womb.120


1. Lead Content Assessment

Data is lacking regarding the exposure from heavy metals used in common building materials. Despite this, lead is known to be persistent, bioaccumulative and toxic (PBT). To reduce the release of PBT chemicals associated with the life cycle of building materials, use third-party-certified building products and materials that contain no intentionally added lead above 100 ppm present in the end product.126

2. Lead Hazard Control

Although policies are in place prohibiting indoor use of lead-based paint, lead exposure from deteriorating lead-based paint, dating from before the 1977 ban, is still the primary source of elevated blood lead, especially in children who exhibit elevated hand-to-mouth behaviors.127 Hand-to-mouth behaviors at the extreme are called Pica, a behavior marked by the consumption of foods with non-nutritional value, such as dirt, paper, and potentially toxic substances like paint chips containing lead-based paint found in the home, and effects an estimated 10–32% of children in the U.S.128 Controlling the hazards of existing lead-based paint, pipes, or other materials through abatement is a critical means of exposure mitigation.

Lead abatement concerns the removal of the building component or paint or the permanent enclosure of lead-based paint hazards. Correct abatement refers to any measure designed to permanently eliminate lead-based paint hazards in accordance with EPA regulations 40 CFR Part 745 pursuant to Title IV of the Toxic Substances Control Act (TSCA). In addition to abatement, the EPA and HUD have established standards for interim controls: temporary measures designed to limit lead exposures due to deteriorated lead-based paint. The EPA provides standard training curriculums and regulations for the training and certification of individuals engaged in lead-based paint risk assessment, inspection, and abatement, as well as performance standards (e.g., lead dust standards) for those supervising projects and conducting clearance examinations.129 130

2. Mercury

Mercury occurs in three common oxidation states mercury(I), mercury(II), and elemental mercury. All forms are toxic, although to different extents and with different effects.131 Elemental mercury is or has been used in thermometers, barometers, and pressure-sensing devices as well as batteries, fluorescent lights, thermostats, industrial processes, refining, and lubrication oils. Inorganic mercury was mostly used in the past in skin-lightening creams and soaps and in latex paint. Many of those uses have been ended or reduced in the U.S. For example, mercury is no longer used in paint, and most batteries are also made without mercury.132 133 134 The majority of emissions of mercury are from combustion of fossil fuels and waste.135

In spite of the fact that, in the United States, agricultural and pharmaceutical uses of inorganic mercury have mostly ceased, mercuric chloride is still used as a disinfectant and pesticide.

Methylmercury is an environmental compound formed from the methylation of inorganic mercury. It is not used commercially. However, it can be formed from inorganic mercury waste in aquatic ecosystems, and become part of the human food chain.136

Free mercury is one of only two elements found in a liquid state at ambient temperature. A heavy, silvery-white metal, it is a better conductor of electricity than of heat. It is also unusual as a metal in that it is volatile at room temperature.137 Until 1990, latex paints contained mercury compounds to prevent fouling, mildew, and bacterial growth during storage.138 In 1990, the EPA banned all interior latex paint containing mercury. In 1991, the ban extended to exterior paints.139

Figure 12: Select mercury containing devices and equipment in building materials.140
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Due to certain inherent properties of mercury, including its low melting and boiling points and its ability to transition between chemical forms, mercury is globally pervasive.137 Exposure to elemental or inorganic mercury generally occurs through occupational activities involving the production, use, or incorporation of the chemicals in products. Vinyl Chloride Monomer (VCM) production, through the use of mercury, makes up the second largest global demand for mercury and accounts for 570-800 annual tones in 2008. Most of this takes place in China and Russia, with China making up 80-90% of global capacity.141 Non-occupational exposure to methylmercury occurs mainly through diet, especially through the consumption of fish and other seafood.137 142 Other exposure to mercury comes via its release in air, water, and soil resulting from the production of the chemical, or processes resulting in mercury as a by-product, including coal-burning power plants, cement production, and certain mining activities.143

Mercury is also used in the manufacture of compact fluorescent light bulbs (CFLs).144 The EPA estimates that on average, CFLs contain about 4 milligrams of mercury in the sealed glass tubing, which creates a potential pathway to exposure in homes and workplaces if a CFL is broken. Comparably, CFLs contain a much smaller amount of mercury than other products, such as older thermometers (containing about 500 mg, the equivalent to over 100 CFLs). Small amounts of mercury vapor are released when a bulb is broken, the use of CFLs helps to reduce overall exposure to mercury by minimizing the number of opportunities for exposure, and maximizing the longevity of the bulb. Manufacturers have also been working to reduce the total amount of mercury found in more advanced bulbs, which will further decrease exposure;144 however, precautions should be taken when handling CFLs, particularly during cleanup.145

Health Effects

Cardiovascular System

Blood pressure and heart rate. Evidence from clinical, occupational, and general population studies suggest inhalation of metallic mercury may affect the cardiovascular system in humans, producing elevations in blood pressure and/or heart rate.146

Nervous System

Nervous system damage. Disorders of the central nervous system are commonly associated with exposure to elemental mercury. Acute effects include, according to the EPA, “tremors, mood changes, irritability, reduction in cognitive function, and slowed sensory and motor nerve function.” Chronic exposure also impacts the central nervous system, producing “increased excitability, irritability and tremors”.147

Occupational studies are the primary source for information on mercury exposure. The acute and chronic effects resulting from exposure to mercury closely mirror each other, and both may become irreversible if the concentration or exposure duration increases.146

Urinary System and Reproductive System

Kidney damage, reproductive organs damage, and developmental effects. The most significant impact of chronic elemental mercury exposure is kidney damage. Animal studies have demonstrated that chronic exposure causes changes in testicular tissue, compromised and lower sperm count, while acute mercury exposure can result in acute renal damage.146 147


1. Mercury Content Assessment

Mercury exposure is largely acute and isolated within the context of indoor exposure and is limited to materials such as old thermometers, novelty jewelry and products that might be found in a school science laboratory and which may result in acute exposure when damaged or broken. While less ubiquitous in the built environment than other toxins, mercury exposure is still cause for concern.136 Data for chronic, low-level, non-occupational, indoor exposure is lacking. Nonetheless, mercury is known to be persistent, bioaccumulative, and toxic (PBT).148

To reduce the release of PBT chemicals associated with the life cycle of building materials, use third-party-certified building products and materials that contain no intentionally added mercury present in the end product.149 150 151

2. Mercury Abatement

Mercury is relatively common within the built environment due to its use in thermostats, electronics, and most significantly, fluorescent lights. Therefore complete removal may not be possible. Replacement and elimination should be the goal where possible; and otherwise, precautions should be taken to lessen the risk of mercury release, especially in the case of fragile products such as lighting. In line with efforts to minimize risk, policies and guidelines must be in place to ensure proper recycling and disposal of mercury-containing products.152

3. Cadmium

Elemental cadmium is a malleable and an easily workable silver-white metal that can be rolled into sheets, formed into wire, and easily soldered. However, cadmium, like most other heavy metals, does not occur in nature in its elemental form. It is always found in a compound with another element, the most common being cadmium sulfide, cadmium carbonate, and cadmium oxide. The element was discovered in the 19th century, making its use relatively recent. Major industrial uses include paint pigments, electroplating or protective plating for metals, and as stabilizers in PVC plastics.153 154

A majority of atmospheric cadmium is the result of human activities, including smelting, fossil fuel combustion and municipal waste incineration. Atmospheric deposition of cadmium in soil exceeds the rate at which it is eliminated, causing an eventual buildup of the chemical in soil.155 The use of municipal sewage sludge on agricultural soil further exacerbates concentrations in soils.153 As a result, the primary source of cadmium exposure for non-smokers is the food supply. A variety of produce, including lettuce, spinach, potatoes, and peanuts are known to contain substantial levels of cadmium.156

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Health Effects

Endocrine System and Respiratory System

Lung cancer. Inhalation is a common route of exposure to cadmium in occupational settings. Associations between cadmium inhalation and lung cancer have been found in cadmium workers.157 Based on these occupational studies, in addition to general population epidemiologic studies and animal studies, cadmium and cadmium compounds are classified as known human carcinogens by the IARC.159 160

Respiratory System

Chronic obstructive pulmonary disease. The WHO and the Organization for Economic Co-operation and Development (OECD) state that chronic obstructive airway disease (also known as chronic obstructive pulmonary disease [COPD]) is associated with “long-term, high-level occupational exposure” to cadmium by inhalation. Similarly, inflammation of lung tissue is also associated with chronic occupational exposures to high levels of cadmium.153 161

Urinary System

Renal tubular dysfunction. The kidney is the principal target organ for cadmium exposure. According to the WHO, cadmium accumulates primarily in the kidneys and has a relatively lengthy half-life, about 10 to 35 years. Associated health effects include renal tubular dysfunction, kidney stones, and kidney cancer.153

Renal tubular dysfunction is characterized by an increase in excretion of low molecular weight proteins in urine resulting from increased cadmium in an individual’s kidney. These effects are generally irreversible.153


1. Cadmium Content Assessment

Unlike lead, cadmium is not restricted for use in paints and coatings as a pigment, as well as a stabilizers in PVC products. Indoor exposure data from such sources is lacking. Cadmium, like most toxic metals, is known to be toxic, persistent, and bioaccumulative (PBT).162 163

To reduce the release of PBT chemicals associated with the life cycle of building materials, use third-party-certified building products and materials that contain no intentionally added cadmium present in the end product.149 150 151

4. Chromium VI

Chromium is a lustrous, hard, brittle gray metal. It is found in the natural environment (i.e., rocks, plants and soil), typically in combination with other elements. Nearly all chromium is commercially extracted from chromite or iron chromium oxide and is very rarely found in its free form. It is found in the environment in two states, known as chromium (III) and chromium (VI). Chromium (III) is less toxic than chromium (VI) and is, in fact, essential to the human body for the metabolism of glucose, fat, and protein. The body is capable of converting some amount of chromium (VI) to chromium (III). Most chromium (VI) compounds rarely occur naturally and usually occur as manufactured products or by-products.164 165

Chromium has a long history in the manufacture of high-volume products such as stainless steel, dyes and paints. While other alloying elements may also be used, chromium imparts unique properties such as heat resistance.137 Chromium can be found in the air, soil, and water, having been released by industrial processes including electroplating, tanning, and textile and chromium product manufacture. Chromium can also be released from power plants including natural gas, oil, and coal plants. Once released, the element tends to persist, most often depositing in soil, where it can change between elemental forms, rather than remain in the atmosphere.166

Non-occupational sources are generally minimal, with the exception of contaminated drinking water. Most of the population is exposed to trace levels of chromium through factory waste emissions in the air, soil, and occasionally drinking water. The estimated average daily intake is less than 0.2 to 0.4 µg from air, 2.0 µg from water, and 60 µg from food.165 Cement dust is another non-occupational, building material-based source of chromium exposure. Exposure in occupational settings is estimated at two orders of magnitude higher than general population exposure.165 167

Health Effects

Endocrine System and Respiratory System

Lung cancer and other respiratory cancers. The target system for toxicity in both acute and chronic exposures involves the respiratory tract.168 169 The EPA has classified chromium (VI) as a known carcinogen; inhalation is associated with an increased risk of lung cancer. Exposure to chromium, or related compounds, is also associated with cancer of the nose and nasal sinuses. The IARC identifies chromium (VI) compounds as carcinogenic to humans.165 169


1. Chromium Content Assessment

Data on indoor exposure to chromium is lacking. However, like other heavy metals, chromium is known to be toxic, persistent, and bioaccumulative (PBT).170

To reduce the release of PBT chemicals associated with the life cycle of building materials, use third-party-certified building products and materials that contain no intentionally added chromium present in the end product.149 150 151

Volatile and Semivolatile Organic Compound–Emitting Materials

Volatile organic compounds (VOCs) comprise a large group of organic chemicals that volatize under ambient conditions, evaporating or sublimating to enter the air due to their low boiling point. Semi-volatile organic compounds (SVOCs) are VOCs that occupy a somewhat higher range of boiling points. Indoor VOC sources are abundant, including building materials such as paints, carpets, adhesives, sealants, coatings, and composite wood products and flooring materials.171 While high levels of some VOCs are detectable by smell, other VOCs have no odor.172 VOCs and SVOCs have a wide range of health effects, from irritation to neurological issues and some are known or suspected carcinogens.173

1. Formaldehyde

Formaldehyde is one of the most recognized, well-studied, and commonly occurring indoor VOCs. Formaldehyde is a colorless gas with a pungent odor at room temperature and high vapor pressure. Although formaldehyde emissions are contributed by both anthropogenic and natural sources, according to ATSDR; combustion processes account directly or indirectly for most of the formaldehyde that enters our environment.174

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Formaldehyde is used mainly in the production of resins used in wood products and as an intermediate in the manufacture of industrial chemicals.176 177 178 Pressed wood products containing urea-formaldehyde are a significant source of indoor formaldehyde emissions.179 These include particleboard used in sub-flooring, shelving, cabinetry and furniture as well as decorative plywood paneling and medium-density fiberboard. Softwood plywood and sterling board produced for exterior construction use phenol-formaldehyde (PF) resin instead. Although formaldehyde is present in both UF and PF resins, PF resin emits formaldehyde at a lower rate than UF resin.180

Formaldehyde concentrations in dwellings can vary according to temperature, relative humidity, and air exchange. Higher temperatures and relative humidity increase emission and exposure, while increased ventilation helps to decrease exposure.181 Indoor air is a chief route of formaldehyde exposure for the general population, with a substantial portion of formaldehyde exposure due to building materials and furnishings that are new or recently applied.181 Emissions from newly installed building materials and products decrease with time.182 For the aforementioned reasons, indoor air has higher levels of formaldehyde when compared to outdoor air; at a range of 25 to 60 µg/m³, compared to natural background concentrations typically < 1 µg/m³ with a mean of about 0.5 µg/m³, and higher annual averages between 1 and 20 µg/m³ ppm in urban areas. Average indoor exposures to FA range between 16 and 32 ppb.183 Highest exposure levels occur in formaldehyde-based resin industries, where workers are exposed to high air concentrations as well as liquid forms (dermal exposure) of the pollutant. Low levels of formaldehyde also occur naturally in a variety of foods, including produce.174

Figure 14: Common building material formaldehyde emission rates.184
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In 2010, the Formaldehyde Standards for Composite Wood Products Act was signed into law. Title VI, added to Toxic Substances Control Act (TSCA), establishes limits for formaldehyde emissions from composite wood products, and parallels standards previously established by the California Air Resources Board (CARB) for products supplied or manufactured for sale in California. In July 2016, the U.S Environmental Protection Agency finalized its Composite Wood rule which applies these same emission standards nationally.185

Figure 15: United States Formaldehyde Standards for Composite Wood Products Act: Pressed board products emission limits and implementation phases.186
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Health Effects

Endocrine System

Nasopharynx and sinonasal cancer. Formaldehyde is known to cause cancer of the nasopharynx and has also shown a role in sinonasal cancer. Due to the known long-term health risks, in 1992, the California Air Resources Board formally listed formaldehyde as a toxic air contaminant with no safe level of exposure.187 188 The California Office of Environmental Health Hazard Assessment has set a No Significant Risk Level of 40 ug/day for formaldehyde. Based on the association with nasopharynx and sinonasal cancer, formaldehyde is classified as a known human carcinogen by the IARC.188

Respiratory System

Respiratory irritation and sensitization. Both acute and chronic exposure to formaldehyde can cause eye, nose, and throat irritation and respiratory sensitization. Other non-cancerous symptoms cited by the EPA and IARC include chest pain, coughing, and wheezing.188 189 Limited studies have also shown an association between occupational exposure and asthma.174

Studies on formaldehyde irritation often come from occupational and volunteer cohorts. Levels of formaldehyde of 0.4 to 3 ppm can produce irritation of the eyes, nose, and throat, while the odor threshold in humans is suspected to be between 0.05 and 1 ppm.175


1. Urea-Formaldehyde Content Assessment

To reduce indoor concentrations and hazards of formaldehyde—especially in the case of furniture, composite wood products, laminating adhesives and resins, and thermal insulation—use third-party-certified building products or materials that contain no intentionally added urea-formaldehyde present in the end product and materials that contain no intentionally added urea-formaldehyde present in the end product.149 190

2. Phthalates

Phthalates are a class of plasticizers that are used as polymer additives to increase the flexibility and transparency of plastics. Phthalates are very high production volume chemicals, with over 470 million pounds produced per year, and chiefly used in polyvinyl chloride plastics (PVC).191 Building materials that contain PVC include carpet backing, flooring, wall coverings, upholstery, and waterproof membranes.192

Depending on the product formulation, phthalates can make up to 40 to 60% of the final product weight.193 The lack of a covalent bond between phthalates and the plastic polymers to which they are added leaves them free to be released into the environment.194 Phthalate compounds can leach, migrate, or volatize from PVC-containing products into air, dust, water, food, and soil. Routes of exposure include inhalation, ingestion, and dermal contact. Phthalates that are more volatile, such as diethyl phthalate (DEP), dimethyl phthalate (DMP) and dibutyl phthalate (DBP), tend to be found in higher concentrations in indoor air, while the heavier, less volatile phthalates, including Bis(2-ethylhexyl) phthalate (DEHP) and benzyl butyl phthalate (BBP), tend to be present on indoor surfaces and dust.194

One of the most well-studied widely used phthalate plasticizers, Di(2-ethylhexyl) phthalate (DEHP), is used to impart flexibility to PVC and vinyl chloride resin (the base monomer used in the manufacture of PVC).195 DEHP is commonly used at about 30% of the PVC product by weight.196 Often used in flooring products, it is commonly present at levels many times higher indoors, especially in household dust, demonstrating the potential of some phthalates to off-gas. Occupational exposure to DEHP both during its manufacture, processing, and use in PVC is reported at levels ranging from 0.02 to 4.1 mg/m³, which are below OSHA’s PEL for DEHP for an eight-hour workday of 5.0 mg/m³. Although occupational exposures can be high, exposure to DEHP through medical procedures including blood transfusions (maximum at 8.5 mg/kg/day) or hemodialysis (maximum at 0.36 mg/kg/day) is significant.197 Blood products stored in plastic and used for transfusions can contain 2 to 1,230 ppm DEHP. Apart from exposure through use of medical equipment, the most common route of non-occupational exposure to DEHP is through food via plastics used in processing and storage. Exposure to DEHP through food is expected at 0.25 milligrams per day (mg/day). Individual exposure estimates in the U.S. range from 0.21 to 2.1 mg/day. Other sources are estimated to be lower. The concentration of DEHP in ambient air is quite low, less than about 0.002 ppb in urban areas. In indoor air, concentrations can be higher than outdoor levels, especially after painting or installing flooring.194 197 198

DEHP that is ingested is rapidly broken down in the gut to two major metabolites: mono (2-ethylhexyl) phthalate (MEHP) and 2-ethylhexanol. Exposure that allows entry of DEHP directly into blood takes longer to clear (e.g., blood transfusions). Because MEHP is poorly absorbed into the bloodstream from the digestive tract, little ends up in the blood. Instead, most of it is excreted through urine and feces. Most ingested DEHP leaves the body within 24 hours through similar routes as MEHP. However, compounds that are absorbed into the bloodstream circulate to other organs are stored in body fat and can end up in breast milk.197 DEHP and its major metabolite, MEHP, were detected in the umbilical cords of 74 out of 84 newborns in a 2003 study conducted in Italy, indicating that exposure to DEHP and its metabolites can occur in utero.199 Another study conducted in 2004 found MEHP in 24% of 54 amniotic-fluid samples.200

In 2008, the U.S. Congress enacted the Consumer Product Safety Improvement Act (CPSIA 2008), which requires manufactures and importers to adhere to limits for lead and phthalates present in products for children aged 12 and under. Phthalate limits restricted under CPSIA include Di(2-ethylhexyl) phthalate (DEHP), dibutyl phthalate (DBP), butyl benzyl phthalate (BBP), diisononyl phthalate (DINP), Diisodecyl (DIDP) and Di-n-octyl (DNOP).201 Because of the toxicity and pervasive human and environmental exposure to a number of phthalate chemicals, the EPA initiated an action plan in 2009 addressing the manufacturing, processing, distribution, and use of eight common phthalates: dibutyl phthalate (DBP), diisobutyl phthalate (DIBP), butyl benzyl phthalate (BBP), di-n-pentyl phthalate (DnPP), di (2-ethylhexyl) phthalate (DEHP), di-n-octyl phthalate (DnOP), diisononyl phthalate (DINP), and diisodecyl phthalate (DIDP).191

Health Effects

Digestive System and Endocrine System

Liver cancer. DEHP has been shown to cause liver tumors in rats and mice models.198 202 The U.S. Environmental Protection Agency classifies DEHP as a Group B2, probable human carcinogen.203 However, according to the IARC, because the known mechanism or route by which DEHP increases the incidence of liver tumors in rats and mice is not relevant to humans, DEHP is considered not classifiable as to its carcinogenicity to humans.204

Reproductive System

Reproductive and developmental effects. Animal studies have shown developmental and reproductive effects following exposure to DEHP including birth defects, decreased fertility, and decreased testicular weight.198 202 205

The effects of phthalates on the reproductive system have frequently been examined in animal studies. Male rats have shown abnormally small or absent reproductive organs. This is worrisome because it is suspected that infants and toddlers have higher levels of DEHP than other subgroups, and as much as 35% of their exposure results from ingestion of DEHP-contaminated dust among other routes such as medical procedures and the diet.205


1. Phthalate Content Assessment

The life cycle impact of common phthalates used in building materials, including their pervasiveness, toxicity, and potential to leach or off-gas, may be problematic.

To reduce the life cycle impact of common phthalate chemicals, use third-party-certified building products and materials that do not contain intentionally added DEHP, DBP, BBP, DINP, DIDP, or DIBP present in the end product over 100 ppm.126 151

3. Halogenated flame retardants

Flame-retardant chemicals bestow fire resistance to materials and products ranging from textiles and electronic equipment to building and construction materials including curtains, electronic casings, household appliances, paints and coatings, and insulation and roof liners.206 A wide range of chemicals is used in flame-retardant products, although most can be classified as being halogenated—that is, containing carbon-bonded halogen atoms (typically, chlorine or bromine bonded to carbon).207 Flame-retardant materials are incorporated into products either via a reactive process or an additive one. Reactive processes produce a bond between the flame retardant chemical and the polymer matrix, thereby locking most of the flame-retardant chemical in the product. Additive processes do not form bonds and therefore increase the risk of leaching.194

Polybrominated diphenyl ethers (PBDEs) are flame-retardant chemicals commonly used in plastics and foam for fire resistance. The annual global production of PBDEs is estimated to be around 67,125 metric tons, across eight worldwide manufacturers located in the Netherlands, France, Great Britain, Israel, Japan and the United States.208 PBDEs, like phthalates, are mechanically mixed into polymers rather than reactively bound, making them more likely to leach into the immediate environment.209 Although comprehensive toxicity data is lacking, a consensus statement of nearly 150 scientists identified PBDEs as a class of compounds that include carcinogens, mutagens, reproductive and developmental toxicants, immune toxicants, neurotoxicants, and endocrine disruptors.210 211 212 In 2009, the Stockholm Convention recognized the chief commercial PBDE mixtures, a technical mixture of different PBDE congeners, POPs.50 213 The convention also called for a global ban on 22 chemicals, all of which are organohalogens and several of which are organohalogen flame retardants. Further, based on a screening-level review of hazard and exposure information, the EPA has issued a chemical action plan for select PBDEs calling for their voluntary phase-out, as well as a Significant New Use Rule (SNUR), which mandates that companies notify the EPA prior to engaging in any “significant new use” of the chemical substance/mixture. A Toxic Substances Control Act (TSCA) Section 4 test rule also requires manufacturers, processors, and importers to conduct health and environmental effect testing of the chemical substances or mixtures.209 214

Figure 16: Global consumption of flame retardants (tons) in plastics by type for 2011.215
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Halogenated flame retardants can enter the environment through manufacturing emissions, during the use phase or recycling of a product, combustion processes, or landfill runoff. PBDEs tend to accumulate in fat and therefore result in food chain contamination, including contaminating human breast milk.209 High levels of exposure are thought to result from sources such as fish, and fatty foods, however, ingestion from dust and leachates are thought to be higher.209 Recent studies determined that Tris(1,3-dichloroisopropyl) phosphate (a halogenated flame retardant also commonly referred to as chlorinated Tris) and Firemaster 550 (a mix of halogenated and non-halogenated flame retardants) can migrate from upholstery foam into indoor dust. Inhaled and ingested dust is a major route of exposure.216 Although PBDEs are known to exhibit very low acute toxicity in animal studies, extrapolation to human effects is poorly understood. Further, the differences in health effects between PBDE compounds that are more brominated in comparison to those that are less brominated is not well understood.209

Health Effects

Digestive System and Endocrine System

Adenomas and neoplastic nodules. Animal studies have shown some evidence of carcinogenicity for decaBDE, a type of PBDE, specifically in the incidence of hepatocellular adenomas (liver tumors) and hepatic neoplastic nodules (liver lesions). Based on results from animal studies, the IARC classifies polybrominated biphenyls (PBBs), another kind of flame retardant, as probably carcinogenic to humans.217

Endocrine System

Thyroid effects. Certain commercial PBDE mixtures and congeners have demonstrated negative impacts on thyroid function in animal studies. The EPA reports that thyroid effects observed in male mice during animal studies include reduced serum levels of the thyroid hormone T4 (thyroxine) and follicular cell hyperplasia, an indication of disrupted thyroid function.218

Disruptions to normal levels of the thyroid hormone T4 can alter maternal or fetal thyroid homeostasis resulting in neurological impairment for the infant, including developmental delays and decreased IQ.218

Nervous System

Neurobehavioral effects. In rodent studies, exposure to individual PBDE congeners has been linked to developmental neurotoxic effects, causing changes in behavior including adult hyperactivity, non-habituating behavior profile, and delayed reproductive and neurobehavioral landmarks.218

Reproductive System

Delayed Pubertal Development. PBDEs with fewer bromine atoms have been found to have “fetotoxic and reproductive effects, to alter expression of estrogen-regulated genes and receptors, and to have anti-androgenic effects in animal tests.” PentaBDE, a PBDE considered more toxic than decaBDE, has demonstrated delayed pubertal development.209218


1. Halogenated Flame-Retardant Content Assessment

The persistence, bioaccumulation, and toxicity (PBT) of many halogenated flame retardants, as well as their potential to off-gas during use, make their use problematic.

To reduce the life cycle impact of halogenated flame retardants (HFR), use third-party-certified building products and materials that contain, to the extent allowable by local code, no more than 0.01% (100 ppm) of the HFR in the following components: window and waterproofing membranes, door and window frames and siding, flooring, ceiling tiles and wall coverings, piping and electrical cables, conduits and junction boxes, thermal insulation, furniture and furnishings, and textiles and fabrics.126 149 151

4. Polychlorinated Biphenyls (PCBs)

Polychlorinated biphenyls (PCBs) are a synthetic mix of individual chemicals and are commonly oily liquids or solids, either colorless or yellow, without discernable scent or taste. PCBs were phased out of production and use in the United States in 1977 due to evidence of environmental persistence and negative health effects. Despite phaseout, PCBs remain fairly ubiquitous and have been found in at least 500 of the EPA’s 1,598 National Priorities List sites.219

Because of their resistance to heat and ability to insulate well, PCBs were used as coolants and lubricants in transformers, capacitors, and other electrical equipment. Products made before 1977 that may contain PCBs include fluorescent lighting fixtures and capacitors (found in older electrical devices), as well as microscope and hydraulic oils. Other exposure sources include electrical equipment and appliances that are more than 30 years old; contaminated food sources, especially fish, meat, and dairy products; and contaminated well water and air (hazardous waste sites).220

Health Effects

Digestive System and Endocrine System

Cancer of the liver and biliary tract. Studies in occupational settings determined PCBs were associated with cancer of the liver and biliary tract. Animal studies on rats demonstrated those that were fed commercial PCB mixtures for the length of their lifetime developed liver cancer. The EPA and IARC classify PCBs as probable human carcinogens.220


1. PCB Abatement

To reduce hazards, projects constructed or renovated between 1950 and 1980 that are now undergoing renovation or demolition must carry out evaluation and abatement in accordance with the EPA’s Steps to Safe PCB Abatement Activities.221

5. Bisphenol A (BPA)

Bisphenol A, or BPA, is a phenolic-based chemical that is the building block of polycarbonate plastics and epoxy resins, which are materials used to make products ranging from baby bottles and plastic food ware to eyeglass lenses, water bottles, and medical devices. Canned food linings and some wine vats also use resins that contain BPA. It is also a critical component in epoxy resins used in high-performance coatings, building adhesives, and fillers.

BPA is one of the highest volume chemicals produced globally. About six billion pounds of the chemical are manufactured each year, and more than 100 tons of BPA are released into the atmosphere during production.222 Although generally stable, polycarbonate plastics can release BPA when exposed to UV light or heat. BPA can also end up in the environment through product use or disposal. Studies have demonstrated that BPA-containing plastics that are used to make baby bottles and reusable water bottles can leach the chemical during use. The general population is exposed to BPA through ingestion of foods in contact with the chemical. Indoor air exposure to BPA is a relatively less important contributor to total exposure estimates.223

Few studies have estimated total BPA exposure. Nonetheless, BPA has been found in dust samples, indoor and outdoor air, sewage leachates, and water samples.224 Between 1999 and 2000, BPA was identified in 41.2% of 139 streams across 30 American states.225 A 2003–2004 National Health and Nutrition Examination Survey (NHANES) conducted by the CDC detected BPA in 92.6% of 2,517 Americans six years or older.226 Occupational exposures of BPA show it has minimal acute effects ranging from eye irritation to skin sensitization; there is, however, very little data on low chronic environmental dose effects on human health.222 227 228

Health Effects

Nervous System

Brain development. While there is limited evidence on the effects of BPA on human health, animal studies have shown that exposure might be a cause for concern in humans. Bisphenol A has demonstrated neurodevelopmental effects at a low dose in animal studies. The extent to which this can be extrapolated to human effects is the subject of ongoing debate and studies.225

Although the extrapolation of results from animal studies to humans is lacking, findings in animal studies have been well documented. They include cortical plate growth disruption caused by accelerating neuronal differentiation and migration, initiated by BPA and inhibition of the thyroid hormone triiodothyronine (T3).229

Reproductive System

Reproductive effects. BPA is determined to be weakly estrogenic. There is limited evidence on the effect of BPA on the reproductive system. Exposure is believed to affect the prostate gland. There is also minimal concern that exposure can affect the mammary glands in females and the onset of puberty.230 High doses in animal studies demonstrate some reproductive or developmental changes. There is debate as to whether the reproductive effects of BPA in animal studies can be extended to human health effects.225


1. BPA Content Assessment

Despite scant research on exposure risk, Bisphenol A is pervasive, biomonitoring surveys suggest exposure is continual. Serum and other body fluid levels indicate that BPA intake may be higher than estimated or certain conditions such as pregnancy enable bioaccumulation in humans, or possibly both. To mitigate hazard in indoor environment, use third-party-certified building products and materials that contain no intentionally added Bisphenol A present in the end product.149 150 151

6. Perfluorinated Compounds (PFCs)

Perfluorochemicals (PFCs) are molecules used in the manufacture of fluoropolymers, which are used largely in the manufacture of waterproofing and protective coatings and constituents of floor polish, adhesives, fire-retardant foam, and electrical wire insulation.231

PFCs are often characterized as persistent; due to their biological and chemical stability, they tend to resist usual environmental degradation processes. Further, because of their water solubility and low volatility, they tend to persist in water and soil, usually migrating from soil to groundwater, where they can be transported long distances.231 Once in the body, PFOA and PFOS tend to remain in the body for extended periods of time, with a half-life of roughly 2 to 9 years. Studies indicate PFCs with those with shorter carbon-chain length break down and exit the body more rapidly.231 Because of their wide distribution and persistence, PFCs have a strong potential for bioaccumulation and bioconcentration. Several PFCs, including perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS), both by-products of other commercial products, are pervasive, and therefore increase the chances of human and animal exposure. PFOS is no longer manufactured in the United States, while PFOA has been undergoing phase-out.231

There is limited data for human exposure sources, but significant sources likely include diet. PFOS was the only PFC shown to bioaccumulate to dangerous levels in fish tissue, a primary source of human exposure to PFOS.

Unlike many chemicals of their class, PFOA and PFOS tend not to accumulate in fat, yet they take a long time to clear the body. The expected elimination half-life of PFOA and PFOS in humans is 3.5 and 4.8 years, respectively.231 232

Health Effects

Digestive System and Endocrine System

Liver cancer. Chronic exposure to PFOS and PFOA in animal studies is associated with formation of tumors in the liver. Further research is necessary to extrapolate to potential human effects.231 While PFOS has not yet been characterized by the IARC, PFOA is considered to be possibly carcinogenic to humans.233

Endocrine System

Thyroid disease. Nationally representative cross-sectional studies have shown that serum levels of both PFOS and PFOA are associated with thyroid diseases in U.S. adults. Additional research is needed to determine the mechanism of how PFCs induce changes in thyroid hormone levels.231

Endocrine System and Urinary System

Kidney and bladder cancer. Epidemiologic studies have associated exposure to PFOS with bladder cancer, although further analysis is necessary to understand the link. A large retrospective cohort study with a sample size of over 6,000 PFOA-exposed employees showed elevated mortality ratios for kidney cancer for male workers. The study noted that additional investigations are needed to confirm the findings of this study.231


1. Perfluorinated Compound Content Assessment

There is limited data regarding indoor exposure to perfluorinated compounds; however, due to their persistence, tendency to bioaccumulate, and toxicity, their use may be problematic. To reduce the life cycle impact of materials containing perfluorinated chemicals, use third-party-certified building products and materials that contain no intentionally added perfluorinated compounds present at levels equal to or greater than 100 ppm in components that constitute at least .01% by mass of furniture or furnishing (drapes/curtains) assemblies.126 151

Organochlorine Compounds

Organochlorines, or chlorinated hydrocarbons, are compounds whose structure contains a combination of carbon, chlorine, and hydrogen atoms.234 Organochlorines include plastics such as PVC and chloroprene; pharmaceuticals; pesticides and herbicides; as well as disinfectants.24

1. Polyvinyl chloride (PVC)

Also referred to as “vinyl,” polyvinyl chloride (PVC) is an organochlorine polymer used in thermoplastic materials. PVC is an odorless, solid plastic, commonly white but also amber or colorless, made from the monomer vinyl chloride.235 Due to durability, ease of assembly, and low cost, PVC is one of the most widely used plastic materials in construction. Over 50% of globally manufactured PVC is used in construction, making it the largest production-volume organochlorine, comprising about 40% of total chlorine production.193 236

Figure 17: Percentage and types of plastics used in construction.237
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Vinyl chloride (VC) is the main constituent used in the production of PVC. The process of making PVC makes use of the gaseous form of the vinyl chloride monomer abbreviated as VCM. Exposure occurs largely through inhalation and minimally through dermal absorption. The current short-term PEL requires airborne concentrations below 5 ppm over a 15-minute period, while the longer term, eight-hour average, is 1.0 ppm.238 239

The concern in the use phase of PVC is that residual or unreacted VCM can remain within the polymer after processing and can leach from the PVC material, for example into water as with PVC water piping. However, most drinking water supplies in the United States do not have high levels of VC; levels are so low they are undetectable. For most of the population, therefore, the estimated daily intake of VC via drinking water is effectively zero. Non-occupational exposure of VCM occurs primarily through inhalation of VCM in ambient air or through ingestion of foods in contact with PVC-based packaging. However, VC in the atmosphere generally degrades, so very low levels of the chemical are present in ambient air, with concentrations commonly around 1 µg/m3 (0.4 ppb). Higher levels of the chemical are present in areas near manufacturing and processing plants, landfills and hazardous waste sites, and range from trace amounts to 1 ppm, with levels as high as 44 ppm in some areas. Ingestion is a more common route of exposure to VC. Due to relatively high mobility, VC can leach into foods in contact with PVC-containing material. To limit this exposure, the U.S. Food and Drug Administration regulates vinyl chloride content of several types of plastics.240

To enhance the properties of PVC, additives are often mechanically mixed into the polymer. Because the additives are not chemically bound, they are prone to leaching. Additives include phthalate plasticizer for flexibility, fillers for improved mechanical properties, stabilizers such as cadmium, and biocides for sterilization. Depending on the formulation of the product, phthalates can comprise 40% to 60% of the final weight of the PVC product.193 236

A modified polymer, chlorinated polyvinyl chloride (referred to as CPVC, chlorinated PVC, post-chlorinated PVC, or polychloroethene) is a thermoplastic material widely used in the construction industry in applications similar to PVCs but where higher heat tolerance and fire performance are required.193 Due to its strength, high stiffness, and cost-effectiveness, CPVC offers an economic solution for a variety of hot and cold water piping systems. CPVC is applied as an inner corrosion liner in water tanks and vessels and commonly used in the production of fire sprinklers. Similar to PVC, significant health hazards of CPVC at the use phase include the leaching of additives.193

While the health risks associated with PVC and CPVC in their use phase are relatively limited, disposal, especially landfill disposal, is problematic.193 PVC and CPVC can leach a number of potentially hazardous chemical additives into soil and water. Concerns regarding the toxicological life cycle of PVC have led many nations to limit or ban its use. Although neither the U.S. nor EU governments currently regulate PVC manufacture or use,193 some proactive companies restrict PVC and VC monomer (VCM) from their products.242 243

Health Effects

Digestive System and Endocrine System

Liver cancer. PVC’s constituent, vinyl chloride monomer (VCM), is a known human carcinogen associated with liver cancer.238 The link between angiosarcoma of the liver, a typically rare form of cancer, and vinyl chloride exposure is well studied in occupational workers. Hepatocellular carcinoma, as well as non-cancer liver damage such as necrosis and cysts of the liver, has also been documented.244

Animal studies have shown that exposure to vinyl chloride (VC) early in life is associated with increased susceptibility to VC-associated cancers in adulthood. Based on this data, the “U.S. ATSDR considers fetuses, infants, and young children as ‘highly susceptible population’ for vinyl chloride exposure.” Vinyl chloride is also considered genotoxic, “causing chemical alterations of DNA in tissues that may lead to cancer,” due to effects studied in adults and on experimental animals during development.244


1. Assessment of Polyvinyl Chloride (PVC) or Chlorinated polyvinyl chloride (CPVC) Plastics and their Additives

Despite the limited health risks associated with PVC and CPVC in the use phase, the life cycle impact of chemicals and additives in these materials may be problematic if not addressed.

To reduce the life cycle impact of the toxic and persistent chemicals used in polyvinyl chloride (PVC) or chlorinated polyvinyl chloride (CPVC), use third-party-certified building products and materials that contain no hazardous chemical additives over 100 ppm. Alternatively, restrict the use of building products and materials that utilize PVC or CPVC.126 149 150 151

2. Chloroprene

Chloroprene is a chemical produced in high volumes, a liquid monomer used almost exclusively in the production of polychloroprene rubber, known by the trade name neoprene. About 60% of CR manufactured is used in the rubber industry. Polychloroprene is used in adhesives and sealants typical of façade work, floor coverings, caulking, laminates, structural assemblies, paneling, roofing, and wall coverings.193

Similar to other organochlorine compounds such as PVC and CPVC, CR-based products contain a variety of potentially hazardous additives that can be released over time. Solvent-based, solution-bonding adhesives derived of CR monomer can contain a mixture of hazardous solvents that can be left in the final product in trace amounts, including toluene and butadiene, usually added in addition to some compounding agents such as lead oxide and thiourea for curing. Modified CR adhesives that use water as a solvent do not possess these hazards.193

Health Effects

Endocrine System

Non-specific cancers. Animal studies have shown tumors form at many different sites after inhalation of chloroprene, including the lungs, oral cavity, kidney, liver, skin and mammary gland among other organs.245 However, human data is limited. Occupational studies conducted on workers exposed to chloroprene have not been consistent in their results regarding cancer, thus chloroprene is categorized by the IARC as possibly carcinogenic to humans.246


1. Chloroprene Content Assessment

Chloroprene (CR) is not a danger in its use phase. The life cycle impact of chemicals used in CR, however, is problematic. To reduce the life cycle impact of materials containing chloroprene, use third-party-certified building products and materials that contain no hazardous chemical additives over 100 ppm.126 149 150 151

3. Isocyanate Based Foams

Isocyanates are chemical compounds that contain an isocyanate group, and typically treated with compounds containing hydroxyl groups to produce polyurethane polymers used in polyurethane foams, polyurethane paints, insulation materials, surface coatings, under-carpet padding, and the like.

Isocyanates have been shown to be highly toxic to the mucous membranes of the eyes, digestive tract, and respiratory system and are also associated with increased incidence of asthma.247 Hazards associated with exposure to isocyanates are occupational, typically occurring through inhalation, although dermal contact can also occur during the handling of liquid isocyanates, a primary chemical group used to manufacture polyurethane.248 Exposure to people in buildings can also occur soon after application of the polyurethane, as unreacted isocyanates volatize.249 250

The most commonly used isocyanates are diisocyanates, comprising two isocyanate groups, and polyisocyanates, typically derivatives of diisocyanates and made up of numerous isocyanate groups. Diisocyanates are a group of low-molecular-weight, ring or linear chained carbon based compounds, which commonly include toluene diisocyanate (TDI), methylene bisphenyl isocyanate (MDI), and hexamethylene diisocyanate (HDI).250 251 Diisocyanate exposure occurs during manufacture (mixing), and can occur during application (foaming) or maintenance work, where exposure of people in building can occur as unreacted isocyanates volatize.250 252 Research shows that about 5 to 15% of those who work with diisocyanates develop occupational asthma, of which only a small portion recover.253

In response to toxicity concerns over the use of chlorinated plastics in construction, other plastic alternatives have appeared on the market. Polyurethane (PU) plastics are a large family of polymers with a wide range of properties, most common in one of two structures: those that comprise largely a polyester-based backbone or a polyether-based backbone.24 PU is found in an array of building materials, including rigid board (and sprayed) foam insulation, flexible foam, coatings and paints, adhesives, sealants, window treatments, and resin flooring, and requires the use of isocyanates for production.24 An estimated three billion pounds of PU plastics are produced globally each year presenting a hazard to occupational workers. In the US alone, an estimated 280,000 American workers are exposed to isocyanates annually.252

Health Effects

Immune System

Hypersensitivity pneumonitis and cancers. Cases of hypersensitivity pneumonitis, commonly flu-like symptoms, muscle aches, and headaches, have been reported in workers exposed to isocyanates. There is some evidence that toluene diisocyanate (TDI) may be a carcinogen.254 Although evidence for carcinogenicity of TDI in humans is insufficient, there was sufficient evidence for the carcinogenicity of TDI in animal testing. TDI was therefore determined to be a possible human carcinogen.254

Animals have been exposed to TDI through gavage and inhalation. Dose-related increases were seen in subcutaneous fibromas and fibrosarcomas in male rats given gavage treatment. In female rats, increased incidence of neoplastic nodules of the liver and fibroadenomas of the mammary glands were seen.254

Respiratory System

Respiratory and mucosal irritation and respiratory sensitization. According to the CDC, “isocyanates are powerful irritants to the mucous membranes of the eyes and gastrointestinal and respiratory tracts”.255 Isocyanate exposure is a leading cause of occupational asthma. Exposure on the job can sensitize workers, triggering asthma attacks upon exposure to even low concentrations of the chemical. Chronic occupational exposure to 4,4’-methylenediphenyl diisocyanate (MDI), used in the production of polyurethane foams, is associated with asthma, dyspnea, and other respiratory issues.256


1. Assessment of Isocyanate Content in Polyurethane

Despite the relatively low exposure to isocyanates from polyurethane in the use phase, occupational exposure and exposure during application can be a problem.

To reduce hazards associated with the production and application of polyurethane materials, use third-party-certified, non-isocyanate-containing polyurethane products.126

Wood Preservatives

Because of its abundance and versatility, wood is one of the most basic and readily used construction materials. However, wood is sensitive to biological attack. Biocides impart preservative treatment to protect wood from degradation as well as certain performance characteristics. The extent to which treated wood is hazardous depends on the toxicological and emission or release profile of the biocides used in mixtures that make up wood preservative. Exposure includes air emission, leaching, and biodegradation processes.257 258

1. Chromated copper arsenates (CCA)

In the 1960s, arsenic, pentachlorophenol, creosote, and other products were commonly employed as wood preservatives.258 However, these were associated with carcinogenic effects and their use was eventually restricted or prohibited. Alternative products, chromated copper arsenates (CCA), were used instead, until they, too, were found to pose serious health hazards. Although the EPA prohibited CCA application for residential use in 2003, some CCA-treated woods are still part of existing construction. Because the preservative is long-lasting, it will be present for decades to come in older wooden structures.258 259

Common chromium- and arsenic-free alternatives to CCA biocides include wood preservatives copper boron azoles (CBA), ammoniacal copper quaternary (ACQ), and copper HDO (Cu-HDO). Copper azoles act as a fungicide and an insecticide. Despite efforts, effective means have not been found to keep borate preservatives from leaching out of wet wood treated with copper azoles.260 ACQs contain copper as a fungicide and an ammonium compound as an insecticide. There are currently four standardized ACQ formulations considered alternatives to CCA treatment.261 However, because of its high copper content, ACQ-treated wood is corrosive when used with steel.262 Cu-HDO is composed of copper and N-cyclohexyl-diazeniumdioxide (HDO) and classified as moderately hazardous.258

CCA, as well as wood preservers pentachlorophenol and creosote, are currently in the United States used in industrial or “heavy duty” applications, including utility pole, piling, and railroad tie construction. The EPA’s Reregistration Eligibility Decision (RED) for these three pesticides involved a review to determine reregistration and health and safety considerations. Health risks concerning occupational exposure to all three preservatives, and ecological exposure to pentachlorophenol and creosote specifically, was identified and all “heavy duty” wood preservative product labels subsequently amended per mitigation measures specified in the RED.261

Health Effects

Endocrine System and Respiratory System

Lung cancer. Leachate from CCA contains arsenic, chromium, and copper. The chromium (VI) used in CCA is a known human carcinogen. Evidence links chromium (VI) most strongly to lung cancer, but positive associations have also been seen with cancer of the nose and nasal sinuses.169 The greatest hazard posed by arsenic-containing biocides may be exposure to arsenic leachate. Although arsenic is found in dietary sources such as shellfish, meat, poultry, and dairy, it is found in its less harmful organic form and at very low levels. However, inorganic arsenic most commonly found in contaminated sources, e.g., leachate, is highly toxic. Numerous studies show that inorganic arsenic can increase the risk of skin, liver, bladder, and lung cancer.263 264 265


1. Assessment of Wood Preserver Content

Despite the low use phase concerns for industrial applications of chromated arsenicals, pentachlorophenol and creosote, the occupational and potential life cycle impacts of these chemicals pose concern.

To reduce the life cycle impact of materials that use the industrial wood pesticides CCA, pentachlorophenol, and creosote, use third-party-certified wood materials that contain no known hazardous biocides in the end product.149 150 151

Alternative Fuels and Raw Materials

Industrial by-products, residue, and waste used as alternative fuels and raw materials in manufacturing processes reduce embedded energy and raw material consumption. Whether waste is reused or recycled in production depends on its properties and combustibility.

Alternative fuels (AFs) and raw materials or substitution combustibles used in clinker manufacture are composed of flammable, high-energy wastes and solid residual fuels (SRFs), such as dried sewage sludge containing plastics, wood, and paper.266 Generally termed alternative fuels (AF) or refuse-derived fuels (RDF), they are an attractive alternative to fossil fuels. Further, energy is not the only thing recovered through the use of residue combustibles. These wastes also contain materials necessary for the making of products like Portland clinker; ash from solid waste and sewage sludge incineration are used up in clinker production.266 267

Figure 18: Composition of Portland cement.268
expand this figure

Use of RDFs can leave trace toxic pollutants in production materials.269 Co-incineration of cement with waste-derived fuels has been shown to increase the toxic load of the final product. Toxic residues in clinker manufacture include lead, cadmium, copper, zinc, and chlorine. The European Commission report on RDFs found significant increases in the toxic load of the end materials cement clinker, gypsum, and fly ash as compared to those made without RDFs.269

Commercial cement also contains recycled admixtures designed to improve both workability and desired end properties.266 gypsum is added to clinker, up to 5% by weight, as well as blast furnace slag from iron metallurgy and fly ash. Although more than 90% of commercial concretes are produced with admixtures, not all of the admixtures are recycled materials. The majority of admixtures are plasticizers or superplasticizers composed of modified organic wastes. While about 80% to 90% of the initial admixture mass becomes part of the cement, the unsorbed portion is subject to reaction or degradation processes that can have damaging environmental and health consequences.266

expand this figure


1. Assessment of Refuse Derived Fuel Residue Content

Although the use of refuse-derived fuels (RDFs) is known to leave traces of toxic pollutants in some building products and materials, hazard of phase exposure is not clear.266

To reduce the concentration of toxicants in cement materials resulting from hazardous fuel sources, including RDFs, as well as known toxic admixtures, use third-party-certified cement materials that are assessed for intentionally added admixtures and residues.149 150 151

Explanations of Solutions

Asbestos Substitutes

The list below of fiber types organized by category and type by the U.K. government’s Health and Safety Laboratory serves as a guide to common fiber substitutes.85 The list also includes, where possible, references to the IARC’s groups of carcinogenicity: Group 1 is carcinogenic to humans; Group 2 is carcinogenic in animal studies, while the number of species and type of study determines whether it is 2A (probably carcinogenic to humans) or 2B (possibly carcinogenic to humans); and Group 3 is fibers considered non-classifiable (inconclusive) as to their carcinogenicity to humans. Asterisks indicate fibers that are high priority for assessment:85

1. Mineral fibers:

2. Plant fibers:

3. Animal fibers:

i. Inorganic material–based

1. Continuous glass filament fibers:

2. Mineral wool fibers * (Group 3):

3. Ceramic or refractory fibers * (Group 2B):

4. Alkaline earth silicate refractory fibers * (Group 3):

5. Metallic fibers:
* Steel, ductile iron, Cu wool fibers, and various other pure metals and metal alloys.

ii. Natural polymer–based fibers

1. Regenerated cellulose derivatives:

2. Regenerated protein fibers:

Synthetic fibers that are based on petrochemical polymers, including common trade name and fiber polymer abbreviation and composition.
i. Synthetic polymer fiber

1. Polyamide

alphatic *:

wholly aromatic Aramid * and Para-aramid*:

aliphatic-aromatic / aromatic heterocyclic polyamides*:

2. Polyester:

3. Polyolefin:

4. Polyvinyl:

5. Polyurethane:

6. Polyimide:

*7. Polyimidazole:

8. Polythiazole:

9. Polyoxazole:

10. Polyhydrazide:

11. Polyazomethine:

ii. Carbon fibers Fibers with over 99% pure carbon produced by pyrolysis:

Asbestos Abatement

For the purposes of regulation, asbestos-containing materials (ACM) are roughly divided into two categories: friable and non-friable.270 Friable ACM describes any material that contains more than 1% asbestos that, when dry, can be crumbled, pulverized, or reduced to powder by hand pressure. Non-friable ACM (also containing more than 1% asbestos) cannot be crumbled, pulverized, or reduced to powder by hand pressure. Under NESHAP, non-friable ACM is further divided into two categories: Category I is rarely friable and includes asbestos-containing resilient floor coverings, asphalt roofing products, packaging, and gaskets; Category II includes all other non-friable ACM.270 271

With the exception of use in certain areas of a building, e.g., boiler and pipe insulation/wrapping, there is no definite way to know whether asbestos is present.272 The only way to determine with certainty that asbestos is present in a building is to conduct a thorough evaluation. The assessment may be conducted by a NESHAP-certified asbestos consultant or the state or local equivalent; by an architect, consulting engineer, state-certified inspector or certified industrial hygienist; or by an EPA-certified company experienced in asbestos assessment. Asbestos-containing material is generally present in three general forms: surfacing material sprayed or spread on ceilings and walls; pipe and boiler insulation; and in miscellaneous materials, such as tile or board products used in ceilings, floors, and walls. Friable ACM is most commonly found in the first two category uses.91 273

Minimizing the health hazards of asbestos depends on the condition of the ACM. It can involve removal, enclosure, encapsulation, or an operations and maintenance plan.274 Depending on the condition of the ACM, removal may be necessary. The advantage to this action is permanence and no need for continued monitoring. Further, since a building containing asbestos cannot be demolished without the removal of asbestos, the solution is a long-term one. However, the cost of complete removal is usually high, as is the replacement of asbestos with safer alternatives. An important aspect to removal is containment of ACM and arrangement for proper disposal.274

Depending on the condition of the ACM, an alternative to removal is enclosure or encapsulation. Enclosure in airtight new construction is cost-effective in the short run.91 But because asbestos fibers will continue to be released behind the enclosure, periodic inspection and repairs will be necessary until the ACM is removed or the building is demolished. Encapsulation requires that the surface of the asbestos-containing materials be covered, commonly in laminate or paint coatings. A common example is the covering of asbestos-containing floor tile with new, non-asbestos-containing vinyl tile. Similar to enclosure, this minimizes the release of asbestos fibers. However, encapsulated asbestos must also regularly be monitored and maintained to ensure deterioration or damage has not occurred. A disadvantage to enclosure and especially encapsulation is the potential increased difficulty for removal of the ACM in the future. Further, the long-term costs may be higher than for immediate removal.91 273

Lead Abatement

Lead-based-paint abatement can take the form of removal, encapsulation, or enclosure. Following any abatement, the hazard should be tested for lead clearance before containment is removed.

Building component replacement involves the removal of building items, including doors, windows, and trim that contain lead-based paint and replacement with items that do not.275 Because it offers a permanent and effective solution, component replacement is an ideal abatement method, although it is not always feasible. When correctly done, it minimizes contamination of the property and worker exposure. All lead-based components must be stored in a secure, locked area, as must all lead-contaminated waste, until disposal.275

Encapsulation isolates lead-based paint through the use of an applied liquid coating or a material that can be adhered as a covering. Although encapsulation can be completed through the use of mechanical fasteners, the typical means of attachment generally require bonding.275 Because successful encapsulation depends on the bond between the encapsulant and existing lead-based-paint material, thorough assessment to determine suitability is required prior to application.275

Enclosure has similar goals to encapsulation, to create a “dust-tight system” preventing exposure. It requires the installation of a mechanically attached and sealed barrier.275 Unlike encapsulation, enclosure does not require the lead-based paint surface to be stable or durable. Enclosures must be designed to last at minimum 20 years. The enclosure process produces little or no hazardous waste and causes minimal degradation of the lead-based-paint surface. An even more minimal level of containment can be applied by mounting an enclosure flush against the lead-based-paint material. Regardless of the method of enclosure, cleanup and clearance is required after the process is complete.275

Removal of lead-based paint requires separating the paint from affected materials, on or off site, using heat guns, chemicals, or abrasion.129 Paint removal is generally limited to areas or cases in which historic preservation is necessary. Due to hazards relating to removal techniques or lead-based-dust exposure, lead-based-paint removal requires the highest level of worker protection, containment, control, and disposal of hazards. It also generates the greatest amount of waste and is the most expensive. Paint removal also generally requires a more extensive cleaning process to meet clearance criteria. Despite these barriers, paint removal has a low re-evaluation or monitoring failure rate.129

Mercury Abatement

Steps outlined in the EPA’s Mercury Management and Exposure Prevention guidelines for schools can be used to identify and eliminate materials considered high hazard for mercury exposure in all buildings.276 The table below of commercial products containing mercury can be used as a guide. High-hazard products are reviewed with regard to use, potential for release, and availability of a substitute. Using these criteria, damaged or obsolete devices and products containing mercury are safely removed, disposed of, and eliminated where possible. Further, spill response measures and cleanup measures are implemented for mercury-containing articles that cannot be removed or eliminated, as well as safe disposal methods.276

Commercial products that may contain mercury:

Polychlorinated Biphenyls (PCBs) Abatement

Abatement of Polychlorinated Biphenyls in a building constructed or renovated between 1950 and 1979 and undergoing present-day renovation or demolition first requires testing for the presence of PCBs in the building.277 A sampling plan is developed to characterize potential building materials that might contain PCBs or be contaminated due to contact with PCB containing materials (e.g., caulk). The sampling plans include documentation and may include sampling of solid, porous, and non-porous materials as well as indoor air. If a PCB problem is identified, it will require characterization and determination of the extent of contamination.278

Abatement activities following testing and characterization must be conducted in accordance with the Environmental Protection Agency (EPA) and OSHA regulations. The work must reduce risk of exposure to workers. Abatement requires a strategy to be developed that potentially necessitates the involvement of a regional PCB coordinator and state environmental health agency. Removal and abatement procedures for contaminated building materials will require classification per outlined guidelines in the EPA’s Building Characterization and Sampling Plan. Further, removal of caulk with PCB concentrations equal or greater than 50 ppm with any attached PCB-containing building materials must be disposed of in accordance with methods provided in 40 CFR 761.62.277 After removal and breakdown, all materials require contained disposal (i.e., that they be wrapped in poly sheeting or placed in a drum) and immediate transportation to a designated storage area. Lastly, the contractor must keep daily documentation of field activities and an abatement report prepared at the end of the project.221 279



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REACH authorization is granted on a case-by-case basis. The process requires manufacturers to prove they can adequately mitigate risks associated with the chemical in question, that use of the chemical provides greater socioeconomic advantages than its disuse, and that there are no comparable substitutes.11 Lastly, REACH Annex XVII provides a list of chemicals that have been restricted and regulated (at least in individual EU member states) prior to the establishment of REACH. A core feature of REACH Annex XVII is to collect and harmonize chemicals that have been restricted through various piecemeal regulations developed over time across various member states.11

REACH places tough restrictions on the types of information manufacturers can claim as confidential and requires greater disclosure of certain information, including basic chemical properties and analytical detection methods that make it possible to identify and determine exposure risks.11 REACH also does not differentiate between chemicals in use prior to the implementation of the regulation and chemicals that come after; the goal is to treat all chemicals equally. All new chemicals have to go through the registration process, while existing chemicals must be registered in phases based on production volume.11

While the EU REACH program has some activity outside of the union, other countries continue to adopt their own regulations on chemicals. China, for example, has adopted new laws that regulate chemicals in a similar approach taken by the EPA in the United States, with a stronger focus on “new chemicals.” In Japan, the Chemical Substances Control Law was enacted in 1973, and similar to the EPA has a division of oversight between new and existing chemicals with particular attention paid toward chemicals that are known to bioaccumulate and/or persist.19

Because tobacco leaves also tend to absorb cadmium from the soil, smoking is expected to double cadmium body burden levels. The amount absorbed from smoking a pack of cigarettes a day is estimated at one to three µg/day. Average blood cadmium levels of New York City smokers have been measured at 1.58 µg/L, while the national average adult blood cadmium level is about 0.38 µg/L.157 OSHA regards whole blood cadmium levels at 5 µg/l or higher to be hazardous.158

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