Full Disclosure Required: A Strategy to Prevent Asthma Through Building Product Selection

Abstract

Asthma rates in the United States have been rising since at least 1980. Today, nearly 26 million people are affected by chronic asthma, including over eight million children. These rates are rising despite the proliferation of asthma control strategies, including indoor air quality (IAQ) programs. The Centers for Disease Control (CDC) reported that the number of people diagnosed with asthma grew by 4.3 million during the last decade from 2001 to 2009. In response to this growing problem, health organizations have identified a number of chemicals that are known to cause the onset of asthma and are therefore labeled asthmagens. Since these chemicals are common ingredients of many interior finishes, like floors, carpets, and paints, it is possible to improve asthma prevention strategies by reducing or eliminating these chemicals from building materials. As asthma affects more people and we identify chemicals that cause asthma, it becomes increasingly clear that new strategies need to be considered, especially in the building industry, that focus on the prevention of asthma onset. Through this report the Healthy Building Network (HBN) examined this larger problem through a three-pronged approach, examining how pervasive asthmagen chemicals are in the built environment, what steps have been taken to address them, and what further actions are needed. HBN makes these recommendations: screen building product contents for asthmagens, continue research to understand fully asthma onset mechanisms and potential exposures to asthmagens from building materials, and modify indoor air quality certification and building rating systems to address asthma.

Introduction

The Global Initiative for Asthma (GINA) defines asthma as a “heterogeneous disease, usually characterized by chronic airway inflammation. It is defined by the history of respiratory symptoms such as wheeze, shortness of breath, chest tightness, and cough that vary over time and in intensity, together with variable expiratory airflow limitation.”¹ Untreated, inflamed lungs become more responsive to various stimuli.

In the United States, 26 million people are affected by chronic asthma. After more than doubling between 1980 and 1995, asthma rates continued to increase, at a slower rate, from 1997 to 2010. The percentage of U.S. children diagnosed with asthma rose from 11.4% of all children in 1997 to 13.6% in 2010.² While increasing percentages of people have been diagnosed with asthma, death and hospitalization rates have declined, by 26% and 24%, respectively, from 1999 to 2009. This success is apparently due to improvements in managing asthma attacks.³

Despite this success, asthma still has a high burden on society. Each year in the United States, the condition leads to approximately 13 million visits to physician offices, 1.8 million emergency room visits, and 500,000 hospitalizations. Asthma accounts for over 14 million lost school days for children and another 14 million lost workdays for adults. Over 3,000 people die from asthma attacks annually.⁴ Between medical costs, lost school and work days, and early deaths, asthma costs the U.S. over 50 billion dollars annually.⁵

Research by the Centers for Disease Control and Prevention's (CDC) National Asthma Control Program, found that “asthma is seen more often among children, women and girls, African Americans, Puerto Ricans, people in the Northeast, those living below the federal poverty level, and those with particular work-related exposures.”⁶ Particularly relevant to those interested in low-income housing are the links between asthma and socioeconomic status, which is also reflected on a global scale. A recent GINA report found that there is, “a higher prevalence of asthma in developed than in developing nations; in poor compared with affluent populations in developed nations and in affluent compared with poor populations in developing nations; are likely to reflect lifestyle differences such as exposure to allergens, infections, diet and access to health care.”⁷ One of the important factors influencing exposure to allergens is the indoor environment, where Americans spend about ninety percent of their lives.⁸

According to Juliana Maantay of the Department of Environmental, Geographic, and Geological Sciences at Lehman College, “dampness, mold, dirty carpeting, and pest infestations are often components of substandard housing, each leading to associated health problems, especially allergy symptoms and exacerbation of asthma attacks in asthmatics.”⁹ The U.S. Environmental Protection Agency's (EPA) Green Building Working group estimates that indoor pollution “may be two to five times higher, and occasionally more than 100 times higher, than outdoor levels.”¹⁰ Building materials are a potential source of this pollution and, as we show below, may contribute to the development of asthma through exposures from before birth to early childhood to adulthood, and can trigger asthma attacks for those who already have the disease.

To identify asthmagens involved in building materials, we compiled a list of chemicals using three commonly referenced asthma lists: the Association of Occupational and Environmental Clinics (AOEC) Exposure Code List, the Commission de la santé et de la sécurité du travail (CSST, the Commission on Health and Safety at Work in Quebec) List of Agents Causing Occupational Asthma, and the Collaborative on Health and the Environment (CHE) Toxicant and Disease Database. We cross-referenced chemicals on this compiled list with those present in building products in the Pharos Project Building Product Library (Pharos BPL).

The Pharos BPL, a project of HBN, evaluates over 1,600 building products and components. The Pharos BPL characterizes a cross-section of interior finishes that can greatly impact indoor air quality, such as paints, adhesives, composite woods, floors, walls, ceilings, and insulation. These evaluations, informed by manufacturer engagement and independent research, provide an extensive reference set of product ingredient data.

Our analysis identified the presence of 50 asthma-related chemicals in building products. The authors reviewed the available scientific and regulatory literature on each, including many of the case studies that asthma experts rely upon for developing the three asthma lists and others like it. Our literature review also revealed emerging evidence for chemicals currently not on asthma lists, for which epidemiological evidence and investigations into new understandings of asthma onset have linked these chemicals to asthma.

In this article, the authors identify gaps in knowledge surrounding the asthma epidemic and provide a new strategy for asthma prevention from building materials by examining: what is known about asthma, the presence and pathways for occupant exposure to asthmagen-causing chemicals in building materials, and current coverage of asthmagens in leading green building standards.

Discussion

How chemicals cause asthma

Disease prevention requires understanding how environmental factors contribute to its development. Asthma develops through a variety of complex mechanisms. Many factors influence the development of asthma including dose, duration, physiochemical characteristics of a chemical (such as molecular structure or particle size), and genetic and other factors pertaining to the individual. Once asthma develops, hypersensitivity to many agents may develop.

As a U.S. Department of Health and Human Services report explains, asthma causes an increase in airway responsiveness to a variety of stimuli and if “untreated, the inflammation may lead to irreversible changes in lung structure, known as airway remodeling.”¹¹

Asthma onset has been broken down into two types: allergic asthma and irritant-induced asthma, which result in the same symptoms, but reflect different pathological mechanisms. A person may present with either type or both types depending upon their exposure to asthmagens.

Allergic asthma is the most common form. It is also called immunologic or sensitizer-induced asthma. It involves an immune system response to an allergic agent (sensitizer).¹² Typically, the initial exposure does not produce immediate symptoms; rather, symptoms develop over time with increased exposure and initiation of the immune response (clinically recognized by creation of specific immunoglobulin E [IgE] antibodies, which elicit airway inflammation). Levels of exposure required to elicit this response and cause asthma are not understood, though some researchers believe the severity of reaction and asthma onset may be resolved if removed from exposure to these asthmagens early on.¹³ Specific mechanisms involving the immune system are understood for some, but not all, sensitizing agents.

While inhalation is the primary route, dermal (skin contact) exposures to sensitizing agents have also been found to result in respiratory sensitization.¹⁴ Once a person has asthma, chemicals can exacerbate their symptoms into full-blown asthma attacks or episodes. The more frequent the episodes, the worse the lungs function.

On the other hand, in irritant-induced asthma, the clinical evidence of asthma is clear, but the immune system is not involved, and scientists are still working to understand the mechanism leading to onset. Asthma symptoms due to an irritant do not generally have a latency period, a delay between stimulus and response, as is seen with sensitizing agents, and “may be caused from a single exposure to the irritant.”¹⁵ However, recently, some have begun to suggest that low level exposures could result in irritant-induced asthma with latency.¹⁶ The levels and frequencies of exposures needed to induce this form of asthma are not well studied.

Emerging evidence of connections between early life exposures and childhood asthma suggests other mechanisms for, and contributing factors to, the development of asthma. Researchers are finding that exposures that occur before (prenatal) and after (postnatal) birth can impair the development of lungs and immune systems.

Children are particularly vulnerable to asthma. The absence of public policies to prevent chemical exposures early in life is responsible, at least in part, for the rising rates of asthma among children, according to public health scientists Philip Landrigan and Lynn Goldman.¹⁷ This vulnerability comes from several factors. Children's developmental processes are easily disrupted and they have more time to develop chronic diseases. Additionally, children are more vulnerable because their bodies are still developing the capacity to produce the enzymes needed to break down and remove toxic chemicals from the body and they have greater exposures to toxic chemicals for their body weight than adults.”¹⁸

One way that childhood exposures may inflict damage is through disruption of hormonal cell signaling that is responsible for lung development and maturation. Chemical agents, such as phthalates and perflurocarbons (Tables 1 and 2), have the potential to bind to receptors in cells that control development. Animal studies have revealed that phthalates can bind to hormone receptors involved in initiating expression of genes involved in development and maturation of a number of tissues, including the lungs. Animal pre- and post-natal exposures to phthalates resulted in changes in airway remodeling and allergen response, which can disrupt lung development and function.¹⁹

Table 1.

High-priority Asthmagen Causing Chemicals

Chemicals in building materials	Lists ^a	Uses in building materials	Exposure pathways for building occupants	Sources (see Appendix A)
ASTHMAGENS ( ^* )
Acid Anhydrides (Maleic anhydride and Phthalic anhydride)	AOEC (Rs), Quebec CSST, CHE (acid anhydrides; S-strong)	Alkyd and epoxy resins used in coatings, including paints, vanishes, adhesive and high performance coatings (HPSs); and rubber flooring	Inhalation of emissions during installation and inhalation, dermal contact, and ingestion of dust from wear of coatings and floors	[¹]
Acrylates (MMA, PMMA, Acrylic Acid, TMPTA)^b	AOEC (Rs), Quebec CSST (MMA and cyanoacrylates), CHE (methacrylates; S-strong)	Paints,^c lacquers, varnishes, insulation binders, fluid applied floors (FAFs), flooring finishes, and countertops	Inhalation of emissions during installation of wet applied products and dermal contact with residual monomers in solid products	[²]
Ammonia hydroxide	AOEC (Rs)	Chalkboard paints and acrylic adhesives	Inhalation of emissions during installation and inhalation, dermal contact, and ingestion of dust from product wear	[³]
Bisphenol A Diglycidyl Ether (BADGE)	AOEC (epoxies; G), Quebec CSST, CHE (epoxy resins; S-strong)	Epoxy adhesives, HPCs, and FAFs	Inhalation of emissions during installation and inhalation, dermal contact, and ingestion of dust from wear of coatings and floors	[⁴]
Ethanolamines (Monoethanolamine; 2- dimethylaminoethanol; Triethanolamine)	AOEC (Rs), Quebec CSST, CHE (ethanolamines; S-strong)	Spray polyurethane foam (SPF), adhesives, insulation binder, and HPCs	Inhalation of emissions during installation of wet applied products and insulations	[⁵]
Formaldehyde	AOEC (G), Quebec CSST, CHE (S-good)	Formaldehyde-based resins used in wide range of materials, including laminates, insulations, wallboard, engineered wood, and acrylic/latex adhesives	Inhalation of emissions during installation and product use	[⁶]
Isocyanates (HDI, TDI, pTDI, pMDI, Pure MDI, and 2,4-MDI)^d	AOEC (G), CHE (isocyanates; S-strong), Quebec CSST (TDI, Pure MDI, and various combinations of TDI, MDI, and HDI)	Polyurethane systems including insulation, binders, FAFs, carpet backing, and foam cushions	Inhalation of emissions during installation of wet applied products and insulation; inhalation and dermal contact with emissions and dusts from polyurethane products	[⁷]
Polyfunctional Aziridine (PFA)	AOEC (Rs) and Quebec CSST	Cross-linking agent (hardener) in wet applied products such as finishes and paints^e	Inhalation of emissions and dermal contact during installation and dust from wear of coatings	[⁸]
Styrene	AOEC (Rs), Quebec CSST, CHE (S-limited)	Carpets, rubber flooring and other styrene-butadiene rubber products, polystyrene insulation, and HPCs	Inhalation of emissions during installation and product use.	[⁹]
Suspected Asthmagens (^)
Phthalates (DnHP, DNOP, DBP, DIDP, BBP, DEHP, Dicyclohexyl Phthalate)^f	CHE (phthalates; S&I-limited) and Quebec CSST (DEHP only)	Various polyvinyl chloride (PVC) products, lacquers, flooring finishes, adhesives, and FAFs	Inhalation, dermal contact, and ingestion of dust during use of the building product.	[¹⁰]

Chemicals that directly cause asthma, per the authoritative list of the Association of Occupational and Environmental Clinics (AOEC).

These chemicals are indirectly associated with asthma onset (evidence includes epidemiological studies, epigenetic research, and findings of early life lung and immune system developmental impacts).

Association of Occupational and Environmental Clinics (AOEC) Exposure Code List: The AOEC Exposure Code List includes asthmagens reported by asthma experts and subsequently reviewed under AOEC criteria. The AOEC list uses “Rs” for sensitizing agents, “Rr” for Reactive Airways Dysfunction Syndrome (RADS) agents, “Rrs” if both a sensitizing and RADS agent, “R” if the substance has been reviewed and the literature doesn't meet the criteria for either type, or “G” for agents generally accepted as asthmagens. Commission de la santé et de la sécurité du travail (CSST) List of Agents Causing Occupational Asthma: The CSST is an organization, based in Quebec, that compiles and analyzes scientific information to provide health and safety information for use by Quebec employers. The Collaborative on Health and the Environment (CHE) Toxicant and Disease Database: CHE's Toxicant and Disease Database summarizes links between chemicals and more than 200 human diseases or conditions, of which sensitizer- and irritant-induced asthma are included. The chemicals are listed in connection with a disease/disorder and are then grouped by the strength of evidence available: strong (S), good (G), or (L) limited/ conflicting evidence.

MMA=Methyl methacrylate, PMMA=Polymethyl methacrylate, and TMPTA=

Currently, the Pharos BLP data has not associated MMA with widespread use in paints. However, a MMA safety assessment shows that MMA use in paints may still be common (“Product Safety Assessment: DOW™ Methyl Methacrylate Monomer,” Dow Chemical Company, November 20, 2010, <http://msdssearch.dow.com/PublishedLiteratureDOWCOM/dh_07f2/0901b803807f2a8f.pdf?filepath=productsafety/pdfs/noreg/233-00665.pdf&fromPage=GetDoc>). Thus far, the disclosure of materials in paints has been limited. HBN will be looking into this issue further to see if MMA is still an issue for paints.

HDI=1,6-Hexamethylene diisocyanate, TDI=Toluene diisocyanate, pTDI=polymeric Toluene diisocyanate, MDI=Methylene diisocyanate, pMDI=polymeric Methylene diisocyanate.

Currently, polyfunctional aziridine is only associated with flooring finishes in Pharos BPL listed products, but occupational asthma case studies report use as a hardening agent in many other wet-applied products including, paints, dyes, adhesives, and other finishes.

DnHP=Di-n-hexyl phthalate, DNOP=Di-n-octyl phthalate, DBP=Dibutyl phthalate, DIDP=Diisodecyl phthalate, BBP=Butyl benzyl phthalate, DEHP=Di(2-ethylhexyl) phthalate.

Table 2.

Other Substances of Concern

Chemical group	Lists ^a	Uses in building materials ^*	Sources (see Appendix B)
Acetic acid, glacial	AOEC (Rrs) and Quebec CSST	Silicone caulking and high performance coatings (HPCs)	[¹]
Ammonia	AOEC (Rr), CHE (I-strong)	Carpet backing, fiberglass insulation, and latex	[²]
Biocides (in particular, Didecyl dimethyl ammonium chloride (DDAC); tetrachloroisophthalonitrile; 1,2-Benzisothiazolin-3-one (BIT); Hexamethylenetetramine; Triclosan^**)	AOEC (Rs; DDAC only), Quebec CSST (Tetrachloroisophthalonitrile, BIT, and hexamethylenetetramine only), CHE (I-limited; tetrachloroisophthalonitrile only)	Treated wood floors and carpets, wet applied products, such as paints and natural oil flooring stains	[³]
Bisphenol A (BPA)	None^**	Epoxies (HPCs, fluid-applied floors [FAFs], and adhesives)	[⁴]
Gum Rosin (Colophony)	AOEC (colophony, G), Quebec CSST, CHE (S-strong)	Linoleum and adhesives	[⁵]
Metal Dusts (Al, AlOx, Ch, Co, Ni, V, ZOx)^b	AOEC (Rs), Quebec CSST (Al, Ch, Co & Ni), CHE (S- strong; except AlOx & ZOx)	Steel and aluminum alloys, carpet backing fillers, and flooring finishes	[⁶]
Perfluorocarbons (PFCs, in particular PFBS and PFHxA)^c	None^**	Stain repellants in carpets and textiles	[⁷]
Polyvinyl Chloride	AOEC (Rs), Quebec CSST, CHE (S-strong)	Resilient flooring, wall protection, ceilings, carpet backing and roofing membranes	[⁸]
Tall Oil Rosin	AOEC (Rs), Quebec CSST	Linoleum and adhesives	[⁹]
Toluene	CHE (I-limited)	Adhesives and lacquers	[¹⁰]
Western Red Cedar, other wood dust and bark	AOEC, Quebec CSST, CHE (Wood dust; S-strong)	Composite wood products and laminates	[¹¹]

As identified by cross-referencing asthmagen lists with over 1,300 products in the Pharos Building Product Library (BPL).

These chemicals are present in building products in Pharos, but are not present on asthmagen lists. However, these chemicals were added to this analysis due to emerging evidence of links to asthma found in scientific literature.

Association of Occupational and Environmental Clinics (AOEC) Exposure Code List: The AOEC Exposure Code List includes asthmagens reported by asthma experts and subsequently reviewed under AOEC criteria.The AOEC list uses “Rs” for sensitizing agents, “Rr” for Reactive Airways Dysfunction Syndrome (RADS) agents, “Rrs” if both a sensitizing and RADS agent, “R” if the substance has been reviewed and the literature doesn't meet the criteria for either type, or “G” for agents generally accepted as asthmagens. Commission de la santé et de la sécurité du travail (CSST) List of Agents Causing Occupational Asthma: The CSST is an organization, based in Quebec, that compiles and analyzes scientific information to provide health and safety information for use by Quebec employers. The Collaborative on Health and the Environment (CHE) Toxicant and Disease Database: CHE's Toxicant and Disease Database summarizes links between chemicals and more than 200 human diseases or conditions, of which sensitizer- and irritant-induced asthma are included. The chemicals are listed in connection with a disease/disorder and are then grouped by the strength of evidence available: strong (S), good (G), or (L) limited/conflicting evidence.

Al=Aluminum, AlOx=Aluminum oxide, Ch=Chromium, Co=Colbalt, Ni=Nickle, V=Vanadium, ZOx=Zinc oxide.

PFBS=Perfluorobutane sulfonate, PFHxA=Perfluorohexanoic acid.

How chemicals can disrupt lung and immune system development

Epidemiological studies on children with asthma are finding links between adverse influences on lung and immune system development as infants and development of asthma later in life.²⁰ At birth, only 30–50% of our alveoli, the air sacs in our lungs responsible for oxygen exchange, are present. After birth, rapid growth of these alveoli occurs. Lung volume doubles by 18 months and again by 5 years of age. Sly et al. reports, “Normal lungs grow along trajectories; however, exposure to inflammatory or irritant stimuli can retard lung growth.”

During this time the infant immune system is also developing. Prenatal and early postnatal immune systems are biased toward producing IgE antibodies that activate inflammatory cells.²¹ Unimpaired, individuals lose this bias in favor of IgG antibodies that protect against sensitization.²² Early exposures to sensitizing agents, such as those found in building materials, thus can disrupt the development of lung and immune systems, leaving airways stunted and the immune system biased toward producing IgE.

Maternal exposures to asthmagens can cause epigenetic changes that have impacts on the child's immune system development and function.²³ In one study, mice were exposed dermally to toluene diisocyanate, a common building material ingredient (Table 1), before becoming pregnant. Their offspring had an increased susceptibility to asthma.²⁴ Epigenetic changes have also been associated with endocrine disrupting chemicals, specifically Bisphenol A and phthalates, although the implications for health impacts such as asthma development are currently unclear.²⁵

These emerging associations of asthma with cellular and epigenetic pathways present an imperative for further research into these mechanisms as a way to prevent and potentially treat childhood asthma.

Identifying asthmagens in building products

As described above, asthma develops as a complex interaction of genetic and environmental factors. Commonly cited factors include: tobacco smoke, mold, dust and dust mites, pet dander, pollen, respiratory infections, occupational chemical exposures, and outdoor air pollution.²⁶ While chemical exposures are discussed in occupational asthma, they are largely left out of the discussion as potential causes of asthma in non-occupational settings, such as housing. However as discussed below, there is a growing body of evidence that shows the presence of these chemicals in building materials and indoor dust, through which building occupants may be exposed.

Two previously published reports have compiled lists of agents in the indoor environment, including building materials, known to cause or exacerbate asthma: Risks to Asthma Posed by Indoor Health Care Environments, a collaboration between the Lowell Center for Sustainable Production at the University of Massachusetts Lowell and Health Care Without Harm, and Healthy Environments, prepared by Perkins and Will for the National Institutes of Health.²⁷ In both reports, lists of asthmagens from government and health organizations were compiled and narrowed to those present in the health care or built environment.

Our research builds upon this research by identifying asthmagens listed in building material contents as reported by building product manufacturers and researchers in the Pharos BPL. We used two lists in common to the previously mentioned reports along with another extensive compilation of occupational asthmagens developed by a Quebec worker health commission.

• The AOEC is a non-profit organization dedicated to “[facilitating] the prevention and treatment of occupational and environmental illnesses and injuries through collaborative reporting and investigation of health problems.” The AOEC Exposure Code List includes asthmagens reported by asthma experts and subsequently reviewed under AOEC criteria. Criteria for designation as an asthmagen include specificity and relevant exposure pathways. Additionally, to determine the type of asthmagen, the AOEC looks for these main clinical indicators in case studies published in scientific journals: specific inhalation challenges with immediate or delayed fall in expiratory flow and/or volume—sometimes called the “gold standard” for diagnosis—evidence of changing airway reactivity in response to exposure and control periods, airway hyperresponsiveness to non-specific stimuli, exposure-related asthma symptoms, and presence of specific IgE antibodies (indicates allergic/sensitizer-induced asthma).²⁸

• The Quebec-based worker health commission, CSST, compiles and analyzes scientific information to provide health and safety information for use by Quebec employers. This information includes a list of occupational asthmagens, based on the extensive occupational asthma research of Moria Chan-Yeung and Jean-Luc Malo, who initially published the Tables of Major Inducers of Occupational Asthma in the 1999 edition of Asthma in the Workplace. The CSST research is well referenced; a review of its sources provided clarifications on potential exposure routes for the substances from materials inside buildings.²⁹

• CHE is a project of Commonweal, a health and environmental research institute in Bolinas, CA. Their Toxicant and Disease Database summarizes links between chemicals and more than 200 human diseases or conditions, of which sensitizer- and irritant-induced asthma are included. The database uses human epidemiological studies, health organization data, such as the California Office of Environmental Health Hazard Assessment (OEHHA), and, in some cases, animal data to inform these chemical lists.

Using these as a guide, we reviewed the available scientific and regulatory literature on each, including many of the case studies that asthma experts relied upon for developing the three asthma lists and others like it.

Our literature review also revealed emerging evidence for chemicals currently not on asthma lists, for which epidemiological evidence and investigations into new understandings of asthma onset have linked these chemicals to asthma. We identified 50 substances in common use in building materials that should be either researched further or prioritized for action. Based upon potential for exposure to building occupants, we determined that at least 28 of the 50 asthma-related chemicals deserve urgent attention (Table 1) and that 22 chemicals require further research (Table 2). In many cases, these chemicals can be avoided through informed selection of interior building products.

Building occupants can be exposed to asthmagens in building materials by several pathways:

• Non-volatile asthmagens on the surface of a building finish (carpet, color, furniture, wall, etc.) may be released from the finish as dust through degradation or abrasion and be picked up through the skin on contact

• Semi-volatile asthmagens may migrate from products on to dust particles by adsorption which may in turn be inhaled, ingested, or come into contact with the skin.

• Volatile and semi-volatile asthmagens may volatilize and be emitted into the air to be inhaled.

These pathways will vary in importance for different asthmagens. For some chemicals the evidence is stronger that they can cause asthma through inhalation, whereas others cause asthma through dermal contact.

We recommend further investigation on whether building products present pathways for building occupants to be exposed to all of the chemicals addressed in this report, such as through emissions, dusts, and dermal contact.

The AOEC considers all substances on their asthmagens list to be disease-causative. Its protocol notes that “the AOEC asthmagen criteria do not reflect a specific exposure scenario, which will alter the risk of asthma from a particular substance (e.g. encapsulated or airborne form, enclosed or open process, low or high concentration).”

The presence of asthmagens in materials inherently represents potential exposures to building occupants. However, for 22 of the chemicals (Table 2), more research is needed to determine whether, in normal conditions of use in building materials, exposure pathways for these substances are as significant as for the 28 chemicals we identify above as top priorities (Table 1) for asthma disease prevention.

Emissions-based building product certification protocols may not adequately address chemicals that cause the onset of asthma

Building product indoor air quality (IAQ) certification systems are designed primarily to reduce occupant exposure to volatile organic compounds (VOCs) to concentration levels below those known to pose a number of health hazards to building occupants, such as cardiovascular, nervous, or reproductive system conditions. Since many VOCs may also exacerbate asthma, these certification systems have been used in strategies to address asthma. However, exposure threshold levels established for VOCs that have been deemed protective against other diseases may not be protective against asthma causation.

Additionally, many asthmagen chemicals are semi-volatile organic compounds (SVOCs) and other compound types that require different test and threshold protocols and are not measured and evaluated by current VOC emissions-specific testing protocols. As a result, many known and suspected asthmagens can be present in and released from products that have earned low VOC emissions certifications. For example, of the 50 chemicals that we discuss in this report, only three are included in both protocols of the two leading IAQ standards.

The building industry utilizes product IAQ certification systems to evaluate and select building products that have low emissions of hazardous chemicals. These certification programs function by measuring emissions from products and determining if the resulting concentrations in a building will be below the concentration levels at which specific human health hazards have not been observed.

Two concentration lists are primarily used for this determination in the United States. Threshold Limit Values (TLVs) are established by the American Conference of Governmental Industrial Hygienists (ACGIH) to provide guidelines for exposures in the workplace. Chronic Reference Exposure Levels (CRELs),³⁰ established by the California Office of Environmental Health Hazard Assessment, are more conservative thresholds that address exposures to a wider range of populations, including infants and children. The TLV and CREL concentration levels are determined based on a large set of human health criteria, but frequently do not include asthma onset.³¹

Our analysis indicates that over 70% of the asthmagens that we have identified in building materials are not presently covered by the leading IAQ testing standards. Of the 50 chemicals we identified in building materials listed in Table 3, 36 (72%) are not covered by either CA 01350 or GreenGuard testing protocols. CA 01350 covers 3 (6%) asthmagens from our list, while GreenGuard covers an additional 11 (28%), including 4 of the 8 phthalates associated with building products in the Pharos BPL. Review of two green building certification programs, Cradle-to-Cradle and Living Building Challenge (LBC), found that product content requirements identify 11 and 17 of these chemicals. Overall, 23 (46%) of the asthmagens identified in building materials are not identified by four leading green building programs.

Table 3.

Coverage of Asthmagens in Green Building Standards

			Green Building Standards Identification
Substance of Concern (CAS No.)	VOC status ^a	Global Automotive Industry Declaration Thresholds ^b	Cradle-to- Cradle (2012) ^c	Living Building Challenge (2014) ^d	California 01350 ^e	GreenGuard Gold ^f
TOP PRIORITY
ACID ANHYDRIDES
Maleic Anhydride (108-31-6)	VOC	0.01% (Renault)	no	no	no	yes
Phthalic Anhydride (85-44-9)	SVOC	0.01% (Renault)	no	no	no	yes
ACRYLATES
Acrylic acid (79-10-7)	VOC	0.01% (BGO)	no	no	no	yes
Polymethyl methacrylate (9011-14-7)	VOC	no	no	no	no	no
Methyl Methacrylate (80-62-6)	VOC	0.01% (BGO)	no	no	no	yes
Trimethylolpropane triacrylate (15625-89-5)	VOC	0.001% (Renault)	no	no	no	no
ETHANOLAMINES
2-Aminoethanol (141-43-5)	VOC	no	no	no	no	yes
Triethanolamine (102-71-6)	SVOC	no	no	no	no	yes
2-Dimethylaminoethanol (108-01-0)	SVOC	no	no	no	no	no
ISOCYANATES
Methylene Bisphenyl Diisocyanate (101-68-8)	SVOC	0.01% (BGO)	no	no	no	no
Methylenediphenyl diisocyanate & related compounds (26447-40-5)	SVOC	0.01% (BGO)	no	no	no	no
Toluene diisocyanate (26471-62-5)	VOC	0.01% (BGO)	no	no	no	no
Polymeric TDI (9017-01-0)	SVOC	no	no	no	no	no
1,6-Hexamethylene Diisocyanate (822-06-0)	VOC	0.01% (BGO)	no	no	no	no
4,4'-MDI homopolymer (25686-28-6)	SVOC	none	no	no	no	no
Diphenylmethane-2,4'-diisocyanate (2,4'-MDI) (5873-54-1)	SVOC	0.01% (BGO)	no	no	no	no
Polymeric MDI (9016-87-9)	VOC	0.01% (BGO)	no	no	no	no
PHTHALATES
Benzyl butyl phthalate (85-68-7)	VOC	0.01% (BGO); prohibited over 0.25%	yes	yes	no	yes
Di-(2-ethylhexyl) phthalate (117-81-7)	SVOC	0.01% (BGO); prohibited over 0.3%	yes	yes	no	yes
Di-n-hexyl phthalate (84-75-3)	VOC	0.1% (Renault)	no	yes	no	no
Dibutyl phthalate (84-74-2)	SVOC	0.01% (BGO); prohibited over 0.25%	yes	yes	no	yes
Diisononyl phthalate (28553-12-0)	SVOC	0.1% (BGO)	no	yes	no	no
Diisononyl phthalate (DINP-1: 68515-48-0) (DINP-2,3: 28553-12-0)	SVOC	0.1% (BGO)	no	yes	no	no
Dicyclohexyl phthalate (84-61-7)	VOC	0.1% (BGO)	no	yes	no	no
Diisodecyl phthalate (117-81-7)	VOC	0.1% (BGO)	no	yes	no	no
Di-n-octyl phthalate (117-84-0)	VOC	0.1% (BGO)	no	yes	no	yes
OTHERS
Ammonium hydroxide (1336-21-6)	VOC	0.01% (BGO)	no	no	no	no
Bisphenol A Diglycidyl Ether (BADGE) (1675-54-3 and 25085-99-8)	Non-volatile	0.01% (BGO)	no	yes	no	no
Formaldehyde (50-00-0, and various compounds)	VVOC	Any level must be reported (GADSL 2014) prohibited over 0.1%	yes	yes	yes	yes
Polyfunctional aziridine (64265-57-2)	VOC	no	no	no	no	no
Styrene (100-42-5)	VOC	0.1% (BGO)	no	no	yes	yes
OTHER POTENTIAL ASTHMAGENS
BIOCIDES
Benzisothiazolin- 3-one (BIT) (2634-33-5)	VOC	0.01% (BGO)	no	no	no	no
Didecyl dimethyl ammonium chloride (DDAC) (7173-51-5)	Non-volatile	0.01% (BGO)	no	no	no	no
Hexamethylenetetramine (100-97-0)	Non-volatile	0.01% (BGO)	no	no	no	no
Triclosan (3380-34-5)	VOC	0.001% (BGO)	no	no	no	no
METAL DUSTS
Aluminum (dust) (7429-90-5)	Non-volatile	no	no	no	no	no
Aluminum oxide (dust) (1344-28-1)	Non-volatile	no	no	no	no	no
Chromium & chromium compounds (dust) (7440-47-3; 18540-29-9 (Chromium VI))	Non-volatile	0.001% (Renault) prohibited above 0.1%	yes	yes	no	no
Cobalt & cobalt compounds (dust) (7440-48-4)	Non-volatile	0.001% (BGO)	yes	no	no	no
Nickel & nickel compounds (dust) (7440-02-0)	Non-volatile	0.001% (BGO)	yes	no	no	no
Vanadium (dust) (7440-62-2)	Non-volatile	no	yes	no	no	no
Zinc Oxide (dust) (1314-13-2)	Non-volatile	0.01% (BGO)	no	no	no	no
PERFLUOROCARBONS
Perfluorooctanesulfonic acid & salts (PFOS [C8], 1763-23-1)	VOC	0.001% (BGO); prohibited over 0.1% (Renault)	yes	yes	no	no
Perfluorooctanoic acid & its salts (PFOA [C8], 335-67-1)	VOC	0.01% (BGO)	yes	yes	no	no
Perfluorohexanoic acid (PFHxA [C6], 307-24-4)	VOC	0.1% (Renault)	no	yes	no	no
OTHERS
Acetic acid, glacial (64-19-7)	VOC	no	no	no	no	yes
Bisphenol A (80-05-7)	VOC	0.01% (BGO)	no	yes	no	no
Colophony (gum rosin) (8050-09-7)	Non-volatile	0.01% (Renault)	no	no	no	no
Polyvinyl Chloride (9002-86-2)	Non-volatile	0.1% (BGO)	yes	yes	no	no
Tall Oil Rosin Ester (8002-26-4)	VOC	no	no	no	no	no
Toluene (108-88-3)	VOC	0.1% (BGO)	no	no	yes	yes
Wood dust, esp. Western Red Cedar (no CAS No.)		no	no	no	no	no

VOC=Volatile organic compound, SVOC=Semi-volatile organic compound.

Global Automotive Stakeholders Group (GASG), (2014). Global Automotive Declarable Substance List (GADSL). Available from: <http://www.gadsl.org>.

Cradle to Cradle Products Innovation Institute, (2013). Cradle to Cradle Certified^CM Product Standard—Version 3.0. Available from: <http://www.c2ccertified.org/images/uploads/C2CCertified_Product_Standard_V3.pdf>.

International Living Future Institute, (2014). Living Building Challenge^SM 3.0: A Visionary Path to a Regenerative Future. Available from: <http://living-future.org/sites/default/files/reports/FINAL%20LBC%203_0_WebOptimized_low.pdf>.

California Department of Public Health, (2010). Standard Method for the Testing and Evaluation of Volatile Organic Chemical Emissions from Indoor Sources Using Environmental Chambers Version 1.1. Updated Feb. 2010. California: Division of Environmental and Occupational Disease Control, Environmental Health Laboratory Branch, Indoor Air Quality Section. Available from: <http://www.cdph.ca.gov/programs/IAQ/Documents/cdph-iaq_standardmethod_v1_1_2010%20new1110.pdf>.

Underwriter Labs, (2013). UL GREENGUARD Certification Program Method for Measuring and Evaluating Chemical Emissions From Building Materials, Finishes and Furnishings. Available from: <http://site.ul.com/global/deu/pages/solutions/standards/accessstandards/catalogofstandards/standard/?id=2821_1>.

For those asthmagens that are covered by leading IAQ testing protocols, the testing thresholds are not designed to be protective for asthma onset even though they are protective against many important health problems, including cancer, reproductive and developmental health, and respiratory problems such as asthma exacerbation.

Currently, there is no one green building certification which can help specifiers avoid asthmagens in building products. However, with further transparency and screening, asthmagens can be identified in building materials, and selections can be made to avoid these chemicals. The global automotive industry has an exemplary screening program through their voluntary Global Automotive Declarable Substance List (GADSL). As shown in Table 3, carmakers require suppliers to declare the presence of 39 of the 50 asthmagens identified in our research. While not yet available for building materials, screening for asthmagens can be accomplished through the use of transparency tools such as the Health Product Declaration (HPD) and the Pharos BPL.

Conclusions

Asthma is a complex disease, for which researchers are still working to determine onset mechanisms. However, the presence of asthmagens in building materials and exposures to building occupants are known, and steps can be taken now to prevent exposures even without this information. A precautionary approach that prevents the introduction of asthmagens from building materials into the indoor environment is both possible and an essential part of the strategy to reduce the rate of asthma onset. These are the key elements of this new strategy:

1. Building owners, architects, and designers should screen building product contents for asthmagens. Our report identified 28 top-priority asthmagens. Using the HBN Priority Building Material Asthmagen List, users can filter products in the Pharos BPL to identify those products without these chemicals.

2. More research is needed to fully understand asthma onset mechanisms and potential contributions of asthmagens in building materials to the increasing incidence of asthma.

3. IAQ testing protocols, building product certifications, and rating systems need to develop new protocols that take asthma onset into account. Our research and analysis showed that current building material healthfulness systems are not designed to prevent asthma onset.

Footnotes

Author Disclosure Statement

The authors have no conflicts of interest or financial ties to disclose.

Appendix A

¹Organization for Economic Cooperation and Development (OECD), “Phthalic Anhydride: CAS No.: 85-44-9,” United Nations Environment Programme, Apr. 5, 2006, <http://www.inchem.org/documents/sids/sids/85449.pdf>. James H. Kim, Herman J. Gibb, Annette Iannucci, “Cyclic Acid Anhydrides: Human Health Aspects,” World Heath Organization, 2009, <http://www.who.int/ipcs/publications/cicad/cicad75.pdf>.

²D. Hiipakka and B. Samimi, “Exposure of Acrylic Fingernail Sculptors to Organic Vapors and Methacrylate Dusts,” American Industrial Hygiene Association Journal 48 (1987): 230–237. M.S. Jaakkola, T. Leino, L. Tammilehto, P. Ylöstalo, E. Kuosma, K. Alanko, “Respiratory Effects of Exposure to Methacrylates Among Dental Assistants,” Allergy 62 (2007): 648–654. S. Geukens and A. Goossens, “Occupational Contact Allergy to (Meth)acrylates,” Contact Dermatitis 44 (2001): 153–159. European Chemicals Bureau, “European Union Risk Assessment Report Methyl Methacrylate,” European Communities, 2002, <http://echa.europa.eu/documents/10162/7c9a0eb6-9b7f-4fd6-846b-d480e8e0003d>. Mark J. Mendell, “Indoor Residential Chemical Emissions as Risk Factors for Respiratory and Allergic Effects in Children: A Review,” Indoor Air Journal 17 (2007): 259–277.

³“Hazardous Substance Fact Sheet: Ammonium Hydroxide,” New Jersey Department of Health, July 2011, <http://nj.gov/health/eoh/rtkweb/documents/fs/0103.pdf>. S. Quirce and P. Barranco, “Cleaning Agents and Asthma,” Journal of Investigational Allerology and Clinical Immunology 20 (2010): 542–550. J.J. Jaakkola and M.S. Jaakkola, “Professional Cleaning and Asthma,” Current Opinion in Allergy and Clinical Immunology 6 (2006): 85–90. “Toxicological Profile for Ammonia,” Agency for Toxic Substances and Disease Registry (ATSDR), Sept. 2004, <http://www.atsdr.cdc.gov/ToxProfiles/tp126.pdf>.

⁴L. Kanerva, T. Estlander, H. Keskinen, R. Jolanki, “Occupational Allergic Airborne Contact Dermatitis and Delayed Bronchial Asthma from Epoxy Resin Revealed by Bronchial Provocation Test,” Eur J Dermatol 10 (2000): 475–7; “Éther de diglycidyle et de bisphénol A,” La Commission De La Santé Et De La Sécurité Du Travail Du Québec, updated Jan. 29, 2009, <http://www.reptox.csst.qc.ca/Produit.asp?no_produit=193938&langue=F>. T. Hannu, H. Frilander, P. Kauppi, O. Kuuliala, K. Alanko, “IgE-mediated Occupational Asthma from Epoxy Resin,” Int Arch Allergy Immunol 148 (2009): 41–4.

⁵William N. Rom, ed., Environmental and Occupational Medicine, Fourth Ed. (Philadelphia: Lippincott Williams & Wilkins, 2007), 439. Oliver Vandenplas et al., “Asthma Related to Cleaning Agents: A Clinical Insight,” BMJ Open 3 (2013), published online Sept. 19, 2013. B. Savonius, H. Keskinen, M. Tuppurainen, L. Kanerva, “Occupational Asthma Caused by Ethanolamines,” Allergy 49 (1994): 877–881. R. Piipari, M. Tuppurainen, T. Tuomi, L. Mäntylä, ML Henriks-Eckerman, and H. Keskinen, “Diethanolamine-induced Occupational Asthma, a Case Report,” Clin Exp Allergy 28 (1998): 358–362.

⁶“OSHA Fact Sheet: Formaldehyde,” Occupational Safety and Health Administration, Apr. 2011, <https://www.osha.gov/OshDoc/data_General_Facts/formaldehyde-factsheet.pdf>. “Final Assessment of Occupational Exposure to Formaldehyde From Composite Wood Products,” U.S. Environmental Protection Agency, Oct. 6, 2011, <http://www.regulations.gov/contentStreamer?objectId=09000064812b2b9a&disposition=attachment&contentType=pdf>. Mark J. Mendell, “Indoor Residential Chemical Emissions as Risk Factors for Respiratory and Allergic Effects in Children: A Review,” Indoor Air Journal 17 (2007): 259–277.

⁷“Minutes of the Webinar/Meeting for 13-February-2013,” Federal Interagency Committee on Indoor Air Quality, accessed Feb. 13, 2013, <www.epa.gov/iaq/ciaq/02_13_13meeting_minutes.pdf>. “OSHA Announces New National Emphasis Program for Occupational Exposure to Isocyanates,” Office of Communications, Occupational Safety & Health Administration, accessed June 25, 2013, <https://www.osha.gov/pls/oshaweb/owadisp.show_document?p_table=NEWS_RELEASES&p_id=24273>. Occupational Safety and Health Administration (OSHA), “National Emphasis Program—Occupational Exposure to Isocyanates,” OSHA Instruction CPL 03-00-017, Last updated June 20, 2013, <https://www.osha.gov/OshDoc/Directive_pdf/CPL_03-00-017.pdf>. Mark Spence, “The Current MDI Industrial Hygiene Data on Spray Foam,” Presentation at the American Chemistry Council Polyurethanes Technical Conference, National Harbor, MD, Oct. 5–7, 2009. David A. Marlow, “Help Wanted: Spray Polyurethane Foam Insulation Research,” NIOSH Science Blog, Mar. 21, 2012 (1:55 p.m.), <http://blogs.cdc.gov/niosh-science-blog/2012/03/21/sprayfoam/>. Wayne Tuang, and Yuh-Chin Yuh, “Asthma Induced by Exposure to Spray Polyurethane Foam Insulation in a Home,” Journal of Occupational and Environmental Medicine 54 (2012): 272–273. Andrew Scurria, “Spray Foam Insulation Class Action Gets Green Light,” Law360, July 8, 2013, <http://www.law360.com/cases/50abf8d3a895c0596d000001/dockets>. Anjali Lamba, “Spray Polyurethane Foam (SPF): EPA Considerations,” Office of Pollution Prevention and Toxics, U.S. EPA, 2013. American Chemistry Council Diisocyanates Panel, “RE: Toluene Diisocyanate (TDI) And Related Compounds Action Plan, RIN 2070-ZA15, April 2011,” Feb. 26, 2013, <http://www.regulations.gov/contentStreamer?objectId=090000648120ceac&disposition=attachment&contentType=pdf>. Henry Willem, and Brett C. Singer, “Chemical Emissions of Residential Materials and Products: Review of Available Information,” Environmental Energy Technologies Division, Lawrence Berkeley National Laboratory, Sept. 2010, <http://epb.lbl.gov/publications/pdf/lbnl-3938e.pdf>. Cheryl Krone, Tom Klingner, and John Ely, “Polyurethanes and Childhood Asthma,” Medical Science Monitor 9 (2003): HY39–43. Robert H. Lim, Mohamed S. Arredouani, Alexey Fedulov, Lester Kobzik, and Cedric Hubeau, “Maternal Allergic Contact Dermatitis Causes Increased Asthma Risk in Offspring,” Respiratory Research 8 (2007): 56–64.

⁸T. Estlander, L. Kanerva, P. Talola, R. Jolanki, and M. Soini, “Aziridine Hardener—a New Sensitizer in the Dyeing of Leather,” Contact Dermatitis 44 (2001): 107–109. John R. Ingram, T. Meirion Hughes and Natalie M. Stone, “Occupational Allergic Contact Dermatitis to Polyfunctional Aziridine Crosslinker in a ‘Tufter,’” Contact Dermatitis 58 (2008): 172–173. L. Kanerva, H. Keskinen, P. Autio, T. Estlander, M. Tuppurainen, and R. Jolanki, “Occupational Respiratory and Skin Sensitization Caused by Polyfunctional Aziridine Hardener,” Clinical and Experimental Allergy 25 (1995): 432–439; L. Kanerva, T. Estlander, R. Jolanki, and K. Tarvainen, “Occupational Allergic Contact Dermatitis and Contact Urticaria Caused by Polyfunctional Aziridine Hardener,” Contact Dermatitis 33 (1995): 304–309; D.H. Garabrant, “Dermatitis from Aziridine Hardener in Printing Ink,” Contact Dermatitis 12 (1985): 209–212. B.G. Cofield, F.J. Storrs, and C.B. Strawn, “Contact Allergy to Aziridine Paint Hardener,” Archives of Dermatology 121 (1985): 373–376. Christopher T. Leffler and Donald K. Milton, “Occupational Asthma and Contact Dermatitis in a Spray Painter after Introduction of an Aziridine Cross-linker,” Environmental Health Perspectives 107 (1999): 599–601.

⁹M. Fernandez-Nieto, S. Quirce, and J. Fraj, “Airway Inflammation in Occupational Asthma Caused by Styrene,” Journal of Allergy and Clinical Immunology 117 (2006): 948–950; J.P. Hayes, L. Lambourn, J.A.C. Hopkirk, S.R. Durham, and A.J. Newman Taylor, “Occupational Asthma Due to Styrene,” Thorax 46 (1991): 396–397. “Toxicological Profile for Styrene,” Agency for Toxic Substances and Disease Registry (ATSDR), Nov. 2010, <http://www.atsdr.cdc.gov/ToxProfiles/tp53.pdf>.

¹⁰John Little, Ying Xu, Elaine Cohen Hubal, and Per Axel Clausen, “Exposure to Phthalate Emitted from Vinyl Flooring and Sorbed to Interior Surfaces, Dust, Airborne Particles and Human Skin,” Environ Health Perspect 118 (2010): 253–258. J.J. Jaakkola, L. Oie, P. Nafstad, G. Botten, S.O. Samuelsen, and P. Magnus, “Interior Surface Materials in the Home and the Development of Bronchial Obstruction in Young Children in Oslo, Norway,” American Journal of Public Health 89 (1999): 188–192. J.J. Jaakkola, P.K. Verkasalo, and N. Jaakkola, “Plastic Wall Materials in the Home and Respiratory Health in Young Children,” Am J Pub Health 90 (2000): 797–799. Y. Ait Bamai, A. Araki, T. Kawai, et al., “Associations of Phthalate Concentrations in Floor Dust and Multi-surface Dust with the Interior Materials in Japanese Dwellings,” Science of the Total Environment 468–469, (2013):147–157. F. Carlstedt, B.A. Jönsson, and C.G. Bornehag, “PVC Flooring is Related to Human Uptake of Phthalates in Infants,” Indoor Air 23 (2013): 32–39. Mark D. Miller and Melanie A. Marty, “Impact of Environmental Chemicals on Lung Development,” Environmental Health Perspectives 118 (2010): 1155–1164. Christopher H. Hurst and David J. Waxman, “Activation of PPARα and PPARγ by Environmental Phthalate Monoesters,” Toxicological Sciences 74 (2003): 297–308. L. Benayoun, S. Letuve, A. Druilhe, et al., “Regulation of Perioxisome Proliferator-activated Receptor Gamma Expression in Human,” American Journal of Respiratory and Critical Care Medicine 164 (2001): 1487–1494. C.G. Bornehag, J. Sundell, C.J. Weschler, et al., “The Association Between Asthma and Allergic Symptoms in Children and Phthalates in House Dust: A Nested Case-control Study,” Environmental Health Perspectives 112 (2004): 1393–1397. B. Kolarik, K. Naydenov, M. Larsson, C.G. Bornehag, and J. Sundell, “The Association Between Phthalates in Dust and Allergic Diseases Among Bulgarian Children,” Environ Health Perspect 116 (2008): 98–103. G. Latini, C.D. Felice, G. Presta, A. Del Vecchio, I. Paris, and F. Ruggieri, “In Utero Exposure to Di-(2-ethylhexyl) Phthalate and Duration of Human Pregnancy,” Environ Health Perspect 111 (2003): 1783–1785. E. Kwak, A. Just, R. Whyatt, R. Miller, “Phthalates, Pesticides, and Bisphenol-A Exposure and the Development of Nonoccupational Asthma and Allergies: How Valid are the Links?,” Open Allergy Journal 2 (2009): 45–50. J. Guo, B. Han, L Qin, et al., “Pulmonary Toxicity and Adjuvant Effect of Di-(2-ethylhexyl) Phthalate in Ovalbumin-immunized BALB/c Mice,” PLoS One 7 (2012): available: <http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0039008>. S.Q. Chen, J.N. Chen, X.H. Cai, et al., “Perinatal Exposure to Di-(2-ethylhexyl)phthalate Leads to Restricted Growth and Delayed Lung Maturation in Newborn Rats,” Journal of Perinatal Medicine 38 (2010): 515–521. C. Bornehag and E. Nanberg, “Phthalate Exposure and Asthma in Children,” International Journal of Andrology 33 (2010): 333–345; N.Y. Hsu, C.C. Lee, J.Y. Wang, et al., “Predicted Risk of Childhood Allergy, Asthma, and Reported Symptoms Using Measured Phthalate Exposure in Dust and Urine,” Indoor Air 22 (2012): 186–99.

Appendix B

¹“Acide Acétique,” La Commission De La Santé Et De La Sécurité Du Travail Du Québec, updated Aug. 6, 2012, <http://www.reptox.csst.qc.ca/Produit.asp?no_produit=521&langue=F>. Occupational Safety and Health Administration (OSHA), OSHA Technical Manual (OTM), Section III: Chapter 2, effective date: Jan. 20, 1999. <https://www.osha.gov/dts/osta/otm/otm_iii/otm_iii_2.html>.

²“Toxicological Profile for Ammonia,” Agency for Toxic Substances and Disease Registry (ATSDR), Sept. 2004, <http://www.atsdr.cdc.gov/ToxProfiles/tp126.pdf>.

³“Tétrachloroisophthalonitrile,” La Commission De La Santé Et De La Sécurité Du Travail Du Québec, updated Aug. 6, 2012, <http://www.reptox.csst.qc.ca/Produit.asp?no_produit=196964&langue=F#Reglementation>. Stefan Gartiser, Heike Lüskow, Rita Groß, ”Thematic Strategy on Sustainable Use of Plant Protection Products—Prospects and Requirements for Transferring Proposals for Plant Protection Products to Biocides,” Environmental Research of the Federal Ministry of the Environment, Nature Conservation and Nuclear Safety, Project No. (FKZ) 3708 63 400, 2012; S.J. Bourke, R.P. Convery, S.C. Stenton, R.M. Malcolm, and D.J. Hendrick, “Occupational Asthma in an Isothiazolinone Manufacturing Plant,” Thorax 52 (1997): 746–748; G. Moscato, P. Omodeo, A. Dellabianca, “Occupational Asthma and Rhinitis Caused by 1,2-benzisothiasolin-3-one in a Chemical Worker,” Occup Med 47 (1997): 249–251; H.H. Gelfand, “Respiratory Allergy Due to Chemical Compounds Encountered in the Rubber, Lacquer, Shellac, and Beauty Culture Industries,” J Allergy 34 (1963): 374–381. “State of the Science of Endocrine Disrupting Chemicals—2012,” World Health Organization (WHO) and United Nations Environment Programme (UNEP), 2013, available from: <http://www.who.int/ceh/publications/endocrine/en/index.html>. Jessica Savage, Elizabeth Matsui, Robert Wood, and Corinne Keet, “Urinary Levels of Triclosan and Parabens Are Associated with Aeroallergen and Food Sensitization,” J Allergy Clin Immunol 130 (2012): 430–460. “Fourth National Report on Human Exposure to Environmental Chemicals: Updated Tables, September 2013,” U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, Sept. 2013, <http://www.cdc.gov/exposurereport/pdf/FourthReport_UpdatedTables_Sep2013.pdf>.

⁴A.J. Spanier, R.S. Kahn, and A.R. Kunselman, “Prenatal Exposure to Bisphenol A and Child Wheeze from Birth to 3 Years of Age,” Environ Health Perspect 120 (2012): 916–920. J.L. Peters, R. Boynton-Jarrett, and M. Sandel, “Prenatal Environmental Factors Influencing IgE Levels, Atopy and Early Asthma,” Current Opinion in Allergy and Clinical Immunology 13 (2013): 187–192. Kathleen M. Donohue, Rachel L. Miller, Matthew S. Perzanowski, et al., “Prenatal and Postnatal Bisphenol A Exposure and Asthma Development Among Inner-city Children,” J Allergy Clin Immunol 131 (2012): 736–742; E. Kwak, A. Just, R. Whyatt, R. Miller, “Phthalates, Pesticides, and Bisphenol-A Exposure and the Development of Nonoccupational Asthma and Allergies: How Valid are the Links?,” Open Allergy Journal 2 (2009): 45–50. S. Yoshino, K. Yamaki, X. Li, et al., “Prenatal Exposure to Bisphenol A Up-regulates Immune Responses, Including T Helper 1 and T Helper 2 Responses, in Mice,” Immunology 112 (2004): 489–495. T. Midoro-Horiuti, R. Tiwari, C. Watson, and R. Goldblum, “Maternal Bisphenol A Exposure Promotes the Development of Experimental Asthma in Mouse Pups,” Environmental Health Perspectives, 18 (2010): 273–277. E. O'Brien, I. Bergin, D. Dolinov, et al., “Perinatal Bisphenol A Exposure Beginning Before Gestation Enhances Allergen Sensitization, but Not Pulmonary Inflammation, in Adult Mice,” Journal of Developmental Origins of Health and Disease, 5 (2014): 121–131. M. Alizadeh, F. Ota, K. Hosoi, M. Kato, T. Sakai, M.A. Satter, “Altered Allergic Cytokine and Antibody Response in Mice Treated with Bisphenol A,” Journal of Medical Investigation 53 (2006): 70–80.

⁵J. Elms, D. Fishwick, E. Robinson, S. Burge, V. Huggins, C. Barber, “Specific IgE to Colophony?,” Occup Med 55 (2005): 234–237. Angelico Mendy, Janvier Gasana, Erick Forno, Edgar Ramos Vieira, Charissa Dowdye, “Work-related Respiratory Symptoms and Lung Function Among Solderers in the Electronics Industry: A Meta-analysis,” Environ Health Prev Med 17 (2012): 183–190. P.S. Burge, A. Wieland, A.S. Robertson, D. Weir, “Occupational Asthma Due to Unheated Colophony,” British Journal Of Industrial Medicine 43 (1986): 449–560.

⁶J.-L. Malo and M. Chan-Yeung, “Agents Causing Occupational Asthma,” Journal of Allergy and Clinical Immunology (2009), 123: 545–550; X. Baur, “A Compendium of Causative Agents of Occupational Asthma,” Journal of Occupational Medicine and Toxicology (2013), 8.

⁷“DuPont Zonyl Fluoroadditives for Coatings, Technical Information,” DuPont, 2003, <http://www.alfa-chemicals.co.uk/documents/Zon56DupontZonylsforCoatings.pdf>. Guang-Hui Dong, Kuan-Yen Tung, Ching-Hui Tsai, et al., “Serum Polyfluoroalkyl Concentrations, Asthma Outcomes, and Immunological Markers in a Case-Control Study of Taiwanese Children,” Environ Health Perspect 121 (2013): 507–513, <https://dx-doi-org.web.bisu.edu.cn/10.1289/ehp.1205351>. Anders Glynn, Urs Berger, Anders Bignert, et al., “Perfluorinated Alkyl Acids in Blood Serum from Primiparous Women in Sweden: Serial Sampling during Pregnancy and Nursing, and Temporal Trends 1996–2010,” Environmental Science and Technology 46 (2012): 9071–9079. “Draft Toxicological Profile For Perfluoroalkyls,” Agency for Toxic Substances and Disease Registry, May 2009, <http://www.atsdr.cdc.gov/ToxProfiles/tp200.pdf>. Fourth National Report on Human Exposure to Environmental Chemicals: Updated Tables, September 2013,” U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, Sept. 2013, <http://www.cdc.gov/exposurereport/pdf/FourthReport_UpdatedTables_Sep2013.pdf>.

⁸“Chlorure de Polyvinyle,” La Commission De La Santé Et De La Sécurité Du Travail Du Québec, updated Apr. 4, 2005, <http://www.reptox.csst.qc.ca/Produit.asp?no_produit=280867&langue=F>. M. Larsson and L. Hägerhed-Engman, “PVC—as Flooring Material—and its Association with Incident Asthma in a Swedish Child Cohort Study,” Indoor Air 20 (2010): 494–450; H. Shu, B.A. Jönsson, M. Larsson, E. Nånberg, C.G. Bornehag, “PVC Flooring at Home and Development of Asthma among Young Children in Sweden, a 10-year Follow-up,” Indoor Air (2013): published ahead of print, doi: 10.1111/ina.12074. “Resilient Flooring - FrickTaber Abrasion Test,” <http://tsac-pvc.obiki.org/servicelife.attachment/301586/Abrasion_Tests_Final.xls>, accessed Nov. 1, 2013. J.J. Jaakkola, P.K. Verkasalo, and N. Jaakkola, “Plastic Wall Materials in the Home and Respiratory Health in Young Children,” Am J Pub Health 90 (2000): 797–799. Y. Ait Bamai, A. Araki, T. Kawai, et al., “Associations of Phthalate Concentrations in Floor Dust and Multi-surface Dust with the Interior Materials in Japanese Dwellings,” Science of the Total Environment 468–469, (2013): 147–157. F. Carlstedt, B.A. Jönsson, and C.G. Bornehag, “PVC Flooring is Related to Human Uptake of Phthalates in Infants,” Indoor Air 23 (2013): 32–39.

⁹“Supporting Documents for Risk-Based Prioritization: Tall Oil and Related Substances Category,” U.S. Environmental Protection Agency, Sept. 2008, <http://www.epa.gov/hpvis/rbp/Cat_Tall%20Oil%20and%20Related_Web_SuppDocs_Sept2008.pdf>.

¹⁰Nathaniel McKeown, “Toluene Toxicity Clinical Presentation,” updated Feb. 8, 2013, <http://emedicine.medscape.com/article/818939-clinical>. “Toxicological Profile For Toluene,” Agency for Toxic Substances and Disease Registry, Sept. 2000, <http://www.atsdr.cdc.gov/ToxProfiles/tp56.pdf>. K. Rumchev, J. Spickett, M. Bulsara, M. Phillips, and S. Stick, “Association of Domestic Exposure to Volatile Organic Compounds with Asthma in Young Children,” Thorax 59 (2004): 746–751, doi:10.1136/thx.2003.013680. Mark J. Mendell, “Indoor Residential Chemical Emissions as Risk Factors for Respiratory and Allergic Effects in Children: A Review,” Indoor Air Journal 17 (2007): 259–277.

¹¹S.M. Brooks, J.J. Edwards, and A. Apol, “An Epidemiologic Study of Workers Exposed to Western Red Cedar and Other Wood Dusts,” CHEST 80 (1981): 30S–32S. S. Vedal, M. Chan-Yeung, and D.A. Enarson, “Plicatic Acid-specific Ige and Nonspecific Bronchial Hyper-responsiveness in Western Red-cedar Workers,” J Allergy Clin Immunol 78 (1986): 1103–1109. M. Chan-Yeung, “Immunologic and Nonimmunologic Mechanisms in Asthma Due to Western Red Cedar (Thuja plicata),” J Allergy Clin Immunol 70 (1982): 32–37. Gene Darling and Kate Oliver, eds., “Wood Dust and Occupational Asthma,” California Department of Public Health,” Jan. 2004, <http://www.cdph.ca.gov/programs/ohsep/Documents/wooddust.pdf>.