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Air a WELLography™
First Edition
International Well Building Institute

Table of Contents

Copyright

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

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

  1. not to remove any copyright or other proprietary notices contained in the Air WELLography™;
  2. not to modify the Air WELLography™; and
  3. not to sell, reproduce, display or distribute the Air WELLography™ in any way for any public or commercial purpose. If you are interested in reproducing, displaying or distributing the Air WELLography™ for any public or commercial use, please contact info@wellcertified.com at International WELL Building Institute PBC.

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

Credits

The International WELL Building Institute also acknowledges the important work of Melcher Media in bringing this document to market in its current state.

Produced By:

Melcher Media
124 West 13th Street
New York, NY 10011
www.melcher.com

President, CEO: Charles Melcher
VP, COO: Bonnie Eldon
Creative Producer: Katy Yudin
Senior Digital Producer: Shannon Fanuko
Senior Editor: David Brown
Associate Editor: Luisa Lizoain
Assistant Editor: Karl Daum

Design & Development by Crush + Lovely

Illustrations by Kaarina Mackenzie and Vita Newstetter

Animations by Vita Newstetter

Melcher Media would like to thank Callie Barlow, Jess Bass, Dylan Butman, Tova Carlin, Maria Gagliano, Barbara Gogan, Luke Jarvis, Weronika Jurkiewicz, David Kahn, Susan Lynch, Sami Melcher, John Morgan, Lauren Nathan, Julia Sourikoff, Tori Spencer, Saif Tase, Zoe Valella, and Megan Worman.

Acknowledgements

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; 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

Nourishment: Sharon Akabas, PhD; Alice 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

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

Discalimer

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 standard.wellcertified.com) 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
  7. Acoustics
  8. Materials
  9. Mind

The Air WELLography™ has the following sections:

Air and the Built Environment, which broadly describes how air quality relates to the human experience in buildings.

Air and the Human Body, which provides an explanation of the biological mechanisms relating to respiration, describing how the body functions under normal, healthy conditions.

Elements of Air, 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.

Introduction

Clean air is vital for optimal health.

Every breath we take—whether in our homes, offices, public spaces, or other settings—should be nurturing and energizing. Achieving the goal of clean indoor air requires professionals and consumers to get involved not just in the conversation but also in the implementation of new approaches.

Borders do not bind air, and often, the quality of the air we breathe is not within our control. Biological or non-biological pollution sources all impact the quality of air that we breathe. Although indoor environments are one place where air can be controlled, it can often be more polluted than the air outdoors. Only through the informed design of space, walls, ceilings, and floor layouts for air flow, selection of building materials, efficient ventilation, and air purification methods can we create spaces that are healthy for all people.

The WELL Building Standard™ (WELL) provides a basis for achieving these goals. A prescription of treatment technologies ensures that air drawn in from outdoors is clean and, once indoors, air flow is available and appropriate. In addition, it provides direction to avoid barriers to air flow and pollutants which could degrade indoor air quality.

Ambient outdoor air pollution is likely responsible for 1 in 8 deaths globally and contributes to an estimated 50,000 premature deaths annually in the U.S. and approximately 3.7 million deaths worldwide.1 2 3

The World Health Organization (WHO) reports even greater numbers, estimating that globally, air pollution contributed to approximately seven million premature deaths in 2012.4

Outdoor air quality is responsible for more than $184 billion environmental and $1.7 trillion health-related expenses in economically developed countries, marking it as a significant and grave concern.3 5 For this reason, building developers, owners, and the people who live, work, learn, and play in buildings must be aware of the dangers of indoor air pollution, as well as informed on how to mitigate the risks of harmful indoor air exposure.6

Approximately 65% of outdoor air particle inhalation occurs indoors.7 Exposure to elevated levels of particulate matter is the leading source of mortality among outdoor air pollutants. The economic benefits of filtration interventions exceed costs in most cases by more than a factor of 10.7 The cost of sick leave attributable to current recommended rates of ventilation is $480 per employee per year and lost productivity on a national scale could be as great as $22.8B USD.8 Since buildings manage indoor air quality by drawing in air from outside, the quality of outdoor air has implications within buildings as well.

Additionally, in 1973, the American Society of Heating, Refrigerating, and Air-Conditioning Engineers published Standard 62 (now 62.1), the guiding standard in the U.S. for ventilation design. This standard, Ventilation for Acceptable Indoor Air Quality, has been the basis or inspiration for many building codes across the country. To achieve its intent of minimizing human exposure to poor indoor air quality, Standard 62.1 describes air exchange rate, HVAC (heating, ventilation, and air conditioning) design, and use of outdoor air quality data when creating a building ventilation system.9

In this WELLography, air pollutants are broken up into biological and non-biological elements. Biological pollutants are by-products of living organisms, including plants, animals, pests, bacteria, viruses, fungi, and protozoa, which may become airborne and eventually inhaled. Non-biological air pollutants are usually derived from commercial, industrial, residential, or transport-related activities, including chemical waste and fossil fuel emissions. In addition to providing information on what is in the air we breathe and how it affects our health, this WELLography provides solutions on how to better leverage air quality within buildings for health and wellness.

Air and the Built Environment

Americans spend up to 93% of their time indoors.6

Many parameters of indoor air quality (IAQ) may be worse than outdoor air due to building construction techniques, off-gassing from modern building materials, and poor ventilation practices. Although concentrations of some common organic pollutants can be two to five times higher indoors than outside, the EPA does not regulate indoor air.10

Figure 1 below highlights some common sources of indoor air pollutants.

FIGURE 1: SOURCES OF INDOOR AIR POLLUTION.11 12
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Outdoor pollution sources, including traffic, construction, agricultural activity, wildfires, and stationary combustion sources such as furnaces and power plants are among the outdoor sources that can negatively affect indoor air quality through the introduction of chemical pollutants and particulate matter (PM).

The building envelope offers some protection against outdoor air conditions, provided the initial design is thoughtful, windows can be closed to prevent infiltration of outdoor pollutants, and air drawn through the building’s ventilation system is adequately filtered. In contrast, when the outdoor air quality levels are favorable, building envelope should promote penetration of outdoor air indoors, given that thermal and acoustic conditions are satisfied. If properly designed, structures made of cement and brick are shown to have substantially lower (as compared to wood-sided structures) indoor ozone levels compared with the concentration outdoors.13 In addition, buildings with more considerable air leakage provide less of a barrier to outdoor ozone,13 and older or poorly constructed buildings have a higher penetration of PM2.5 (particulate matter smaller than 2.5 µm).14 In many cases, a building’s windows should have the option of being opened or closed to allow individuals to manage air flow, temperature, and overall comfort within a space. In environments where outdoor air quality is low, however, operable windows may not be the ideal option for preserving occupant health.

Indoor combustion sources, such as candles, tobacco smoke, stoves, furnaces, and fireplaces can release pollutants, including CO, NO2, and fine particulates, into the air.12 Building materials, furnishings (e.g., carpets and furniture finishes), fabrics, cleaning compounds, office equipment, adhesives, solvents, and air fresheners can all emit volatile organic compounds or semi-volatile organic compounds (VOCs and SVOCs) into the indoor environment.10 If sustained at unsafe exposure for long periods of time, these types of air-quality issues can lead to “sick building syndrome,” which involves various nonspecific symptoms such as eye, skin, and upper airway irritation, headache, and fatigue. Often, no disease or other cause of an ailment can be identified, yet acute health effects are linked to time spent in a building.15

Improper maintenance and poor structural or design elements can result in the accumulation of biological particles responsible for a range of adverse health effects. Water leaks, poor plumbing, and poorly ventilated bathrooms can create standing water in which microorganisms, such as bacteria and mold, can breed.16 For example, standing water in air-conditioning systems is associated with past outbreaks of Legionnaires’ disease.17 Furthermore, high humidity environments provide the conditions that are necessary for mold and bacteria growth and survival. Moisture-driven mold colonies can give rise to biologically derived allergens, such as spores and mycotoxins, which, depending on the mold species, can be extremely harmful.18 Humid environments are also hospitable to a range of other organisms, including dust mites and other tiny arthropods.19

Indoor air quality can be properly managed by thoughtful building and HVAC design, avoiding sources of indoor air pollutants that maintain harmful exposure levels, minimizing the infiltration of outdoor pollutants, and air filtration (especially if initial design is inadequate) either through natural ventilation, such as wind and buoyancy, or through mechanical (forced) ventilation systems.20

Air and the Human Body

Respiration is necessary to live. Unfortunately, the same process that sustains us is also an opportunity for airborne pathogens and natural/human-made pollutants to enter the body.

The Atmosphere

Earth’s atmosphere consists of nitrogen (N2) and oxygen (O2), small amounts of carbon dioxide (CO2), and an array of noble gases. Nitrogen is largely inert and is the most common atmospheric gas, accounting for approximately 78% of the atmosphere. Oxygen makes up about 21% of the atmosphere and is necessary for cellular respiration, the process by which energy is generated from the oxidation of nutrients. Carbon dioxide is a trace gas found at concentrations of 330–400 parts per million (ppm). Approximately 1% of the atmosphere is comprised of noble gases that do not take part in naturally occurring chemical reactions.21

Human Respiratory System

In humans, aerobic respiration occurs through the process of breathing, which delivers oxygen to the body’s tissues and cells.22 The human respiratory system is a combination of muscles, organs, and tissues responsible for breathing (Figure 2). Ventilation, another term for breathing, draws air into the lungs, where gas exchange occurs between the alveoli (small gas exchange sacs) of the lungs and the circulatory system.22 Blood then carries oxygen molecules, now bound to hemoglobin (an iron-containing protein in red blood cells) to body tissues where oxygen is needed for cellular respiration.22

This respiratory system can be generally divided into three parts: 1) the upper respiratory tract, which is composed of the mouth, nasal cavity, and pharynx (nasopharyngeal region); 2) the conducting airways, which are composed of the trachea, pulmonary bronchi, and 3) non-respiratory bronchioles (tracheobronchial region); and the gas exchange area of the alveolar capillary bed (alveolar region).22 The upper respiratory tract regulates the entrance and conduction of external air into the body, and the lower respiratory tract, ribs, intercostal muscles, and diaphragm assist with ventilation.22

Figure 2: The human respiratory system.22
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Ventilation is controlled by two components of the autonomic nervous system: the breathing center in the medulla oblongata and pons of the brain stem.22 These brain regions are responsible for establishing and maintaining the rhythm of breathing, or ventilation rate, as well as heart rate and involuntary reflexes. Additionally, they integrate information from stretch receptors in the lungs and accessory respiratory muscles, as well as chemoreceptors in the aorta and carotids, in order to adjust the ventilation rate in response to physical activity and the concentration of dissolved gases and acidity of the blood. Breathing is controlled mainly without conscious thought; however, humans can exhibit voluntarily control over the breathing process.22

Ventilation in the lungs is divided into two phases: inhalation and exhalation.22 Inhalation begins as the diaphragm and the intercostal and accessory muscles expand the thoracic cavity to create a negative pressure, thus drawing air inward. Exhalation occurs as the diaphragm and intercostal muscles relax and the volume of the thoracic cavity decreases, thereby creating a positive pressure and forcing air out of the lungs.22

During inhalation, air containing nitrogen, oxygen, carbon dioxide, and noble gasses enters the body through the upper respiratory tract and is drawn down to the lower respiratory tract.22 There, oxygen passes through the lining of the alveoli into the bloodstream, carried by hemoglobin. Oxygenated red blood cells travel through the arteries, arterioles, and capillaries to the tissues to deliver oxygen and simultaneously pick up CO2, a by-product of cellular respiration. The deoxygenated, CO2-rich blood is carried back to the lungs through the veins where it diffuses across the alveoli, thereby transferring CO2 to the lungs so it can be released from the body during expiration.22

Lung volumes differ by age, gender, and height. Infants and children have higher resting metabolic rates and breathe more air per kilogram of body weight, and therefore the volume of pollutants inhaled is higher than that of adults.23 The oxygen consumption rate of an infant (aged one week to one year) is 7 ml/kg/minute, while the rate for an adult is 3–5 ml/kg/minute. Coupled with the incomplete development of particle removal systems, infants and children are more vulnerable to pollutants per kilogram of body weight and are at risk for the adverse effects of poor air quality.23

Airborne Toxin Exposure and Some Common Health Conditions

The nose and throat are anatomically designed to intercept large particles from traveling deeper into the body. Mucus and cilia (small hairs lining the nasal cavity and upper airways) trap particulate matter and sweep it away before it reaches the lungs.22 However, particles smaller than 10 µm (PM10), and especially ultrafine particles (also known as PM0.1 or nanoparticles) and adsorbed toxicants may be able to bypass these first lines of defense and penetrate deep into the lungs, potentially initiating adverse health effects.24 25

Humans of all ages are susceptible to the deleterious effects of airborne pollutants, which can cause various forms of cellular damage, including cancer.26 The windows of development during gestation and childhood are particularly critical stages, as inhaled chemicals may change the way in which genes are expressed. Prenatal exposure to airborne environmental toxicants, such as fossil fuels, diesel exhaust particles, and ozone, can lead to reductions in fetal growth and cognitive functioning.27 The epigenetic effects of these types of exposure, even at minute levels, can have long-term implications on human health.28

The adverse health effects of poor air quality are widespread. For example, asthma is a prevalent chronic lung disease that affects about 25.5 million people in the U.S.—including one out of 12 U.S. adults.29 30 Asthma has been on the rise in the U.S. since 1980, partially due to the prevalence of asthma triggers within the indoor environment.31 While the exact cause of asthma is unknown, it is thought to be triggered by a combination of genetic factors and aggravation from airborne environmental allergenic particles. Additionally, air pollution such as ozone and particulate matter can make asthma symptoms worse and trigger attacks.32

Allergic rhinitis is a collection of respiratory irritation symptoms—mostly in the respiratory system, nose, and eyes—that can be triggered by allergenic particles, such as pollen or pet dander.29 In the U.S. alone, it is estimated that allergic rhinitis (allergy symptoms), mostly caused by inhalation exposure to pollen, results in $2.4 to $4.6 billion in indirect costs via losses in at-work productivity.33 Numerous studies have shown that allergic rhinitis negatively impacts quality of life, productivity, missed work days, physical activity, sleep, and overall performance. While allergic rhinitis has been considered clinically benign in children, it has been found to impact their performance in school negatively.34

Elements of Air Contaminants

The elements described below are divided into two main categories: elements of biological air contaminants and elements of particulate matter and gasses.

Particulate Matter Derived from Plants and Animals

Particulate matter derived from plants and animals includes pollen and pet dander. These particles often contain reactive surface proteins, which when aerosolized cause adverse immunological or allergic responses in sensitive individuals. According to the U.S. National Institute of Allergy and Infectious Diseases (NIAID), symptoms of environmental allergies include watery eyes, stuffy/itchy nose, coughing, and asthmatic symptoms such as tightness in the chest.35

1. Plant- and Animal-based Particulates

The most common plant-based particle is pollen. Pollen particles are produced by the male reproductive organs in plants and are freely disseminated in the atmosphere as a method of plant reproduction. Pollen particulate can provoke an immune response in some people, thereby inducing an allergic reaction that includes sneezing and cold-like symptoms. Due to pollen’s association with the reproductive cycles of plants, the type and amount of pollen in the air vary by season.36

There are currently no broadly accepted standards explicitly addressing pollen, and methods of monitoring pollen vary by organization. The NAB has a certified testing protocol that identifies the species from which the pollen originates. However, due to the difficulty in conforming to this protocol, there are fewer than 100 sampling sites in the U.S.37 The sampling stations report pollen counts per cubic meter (pcm), as well as the predominant species. The NAB has established qualitative ratings based on pollen counts: 1) “low,” roughly defined as less than the 50th percentile; 2) “moderate,” levels between the 50th and the 75th percentile; 3) “high,” levels between 75th and 99th percentile; and 4) “very high,” levels as those above the 99th percentile.38 In Europe, the Medical University of Vienna is developing a continental pollen map for different plant sources. The methodology for developing this map will establish a threshold for adverse reactions using information collected from pollen diaries kept by 29,000 seasonal allergy sufferers.39

Health Effects

Respiratory System

Asthma. The AAAAI notes that proteins in pet dander, saliva, urine, and skin flakes can aggravate asthma in susceptible individuals.40 Additionally, the Asthma and Allergy Foundation of America (AAFA) recognizes pollen as a trigger for asthma in susceptible individuals.41

Allergies. The AAAAI notes that the proteins in pet dander, saliva, urine and skin flakes can cause an allergic reaction in susceptible individuals. The symptoms may include sneezing, itchy and watery eyes, and sniffling.40 The symptoms of pollen allergies may include coughing, dark circles under the eyes, itchy nose and/or throat, postnasal drip, runny or stuffy nose, sneezing, and swollen, itchy, and watery eyes.41

Nervous System

Weakness and depressed mood. Psychoneuroimmunology and genetic research suggest that allergic reactions to ragweed pollen can cause biochemical changes that directly affect the central nervous system. The release of inflammatory cytokines (small proteins released by immune cells to recruit a reaction to a stressor or damage) directly affects the central nervous system, inducing mental fatigue, lethargy, and depressed mood, which ultimately affect the overall ability to concentrate or be productive.42

Solutions

1. Media Filtration

Filtering incoming air is an effective defense against plant- and animal-based allergens. Filters with a minimum efficiency reporting value (MERV) rating of one to four are targeted to remove particles, such as pollen, that are 10 µm in diameter or larger. Filters with a rating of eight will remove at least 70% of all particles that are 3–10 µm in diameter, which includes cat and dog dander.43 Additional defenses against particulates include not allowing pets on furniture, routine vacuuming of furniture and carpets, or having pets remain outside.44

2. Dust Mites, Cockroaches, and other Pests

Although neither dust mites nor cockroaches are inherently dangerous animals, their droppings contain allergens that can trigger an allergic response in susceptible individuals (Figure 3).45 46 In addition to being allergens themselves, pest feces can act as carriers for other pathogens and toxins and are a major cause of asthma prevalence.45 46 Other pests, especially rodents, produce dander and droppings that similarly cause adverse health effects in humans.45

FIGURE 3: SYMPTOMS DUE TO EXPOSURE TO DUST MITES AND COCKROACHES.45 46
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There are currently no broadly accepted air quality standards specifically addressing allergenic particulates caused by indoor pests. However, the Consumer Product Safety Commission (CPSC) and the American Lung Association (ALA) advise that indoor spaces be regularly cleaned to prevent the spread of these pollutant sources.45

Health Effects

Respiratory and Immune System

Allergies. Proteins in dust mite waste, as well as cockroach bodies, feces, and saliva can cause allergic reactions in susceptible individuals.47 48 Individuals with asthma, chronic stuffy nose or sinus infection, ear infection, and skin rashes are more likely to be allergic to cockroaches, and those with chronic severe bronchial asthma are most likely to have cockroach allergies.48

Asthma. The AAFA notes that materials in cockroach bodies, feces, and saliva can trigger asthma in susceptible individuals. Individuals allergic to cockroaches can develop acute asthma attacks after inhaling air that contains cockroach allergen, with symptoms lasting potentially for hours.48 About 23% to 60% of people with asthma who live in urban environments also have a sensitivity to cockroach allergens.48

Solutions

1. Dehumidification

Controlling indoor humidity with dehumidifiers can help to limit the growth of dust mites.49 50 Additionally, dehumidification is recommended by the Agency for Toxic Substances and Disease Registry (ATSDR) to improve air quality and reduce airborne allergens.51

2. Source Reduction

Combating the infiltration of pests without the use of products that may exacerbate other respiratory symptoms requires a holistic approach to pest management. Integrated pest management (IPM), the method currently recommended by the EPA, involves removing sources of pest food, water, and shelter by routine inspection, maintenance of facilities, and a regular sanitation schedule.52

3. Pest Prevention

Maintaining a hygienic environment helps to prevent pest problems. Some common preventive measures include ensuring that all food and water is stored in bags or containers and is not left out in open areas. In addition, fixing water leaks, limiting clutter, and sealing holes where pests can live and breed helps reduce the likelihood of dust mite and cockroach problems.52

Microbial Pathogens

Microbial pathogens of viral, bacterial, and fungal origin can directly cause a variety of adverse health conditions in susceptible individuals. The immune system is the primary means of defense against pathogens and other stressors. Exposure to pathogens can cause illnesses that range from mild inflammation to life-threatening medical conditions. Poor air circulation and excessive humidity are important variables that contribute to the accumulation and growth of microbial pathogens indoors.

1. Bacteria

Certain species of bacteria can cause pulmonary inflammation and may lead to infection. Bacterial bioaerosols are suspensions of microscopic biological particles that thrive in conditions with poor air circulation and ventilation. They are responsible for illnesses such as tuberculosis and Legionnaires’ disease.53

Health Effects

Respiratory System

Pneumonia, respiratory failure, death. Legionnaires’ disease is a potentially fatal form of pneumonia caused by inhaling the Legionella bacteria in aerosol form, commonly in mist contaminated with the bacteria.54 Legionella can cause serious and life-threatening complications, including respiratory failure, septic shock, and acute kidney failure.54 The CDC estimates that 8,000 to 18,000 hospitalizations occur in the U.S. due to Legionnaires’ disease, of which 5% to 30% result in death.55 Common sources of Legionella are cooling towers, hot tubs, large central air-conditioning systems, and fountains.56

Tuberculosis (TB). TB is spread through the air from person to person when an infected individual coughs or sneezes and generates airborne water droplets.57 The bacterium is carried in the droplets of water expelled from the nose or mouth, which can then be inhaled by an uninfected person nearby. Once aerosolized, TB bacteria can stay suspended in the air for several hours.58 Up to 40,000 droplets are expelled in a single sneeze, and it only takes as few as 10 microbes to cause an infection.59

In the early 1900s, tuberculosis caused one out of every seven deaths in the U.S.57 TB symptoms include fever, chest pain, and a bad cough lasting three weeks. Many people who have tuberculosis remain healthy as the disease lies dormant, but their condition rapidly deteriorates if their immune system becomes compromised.57

Immune System

Humidifier fever. Humidifier fever is a form of sick building syndrome of mixed etiology that can be caused by bacteria in the humidifier system. It includes flu-like symptoms, such as fever, headache, chills, coughing, and tightness in the chest. Humidifier fever usually occurs a few hours after exposure and is often due to the bacteria found in the humidifier reservoir.60 61

Solutions

1. Dehumdification

Controlling indoor humidity via the use of dehumidifiers can help to limit the growth of problematic bacteria.49 Additionally, dehumidification is recommended by the ATSDR to improve air quality and reduce airborne allergens.51

2. Source Control

Any reservoirs used for containment of water that will be aerosolized (e.g., a humidifier) should be cleaned and properly dried between uses to prevent bacterial growth.62

3. Media Filtration

Filters with MERV ratings of 13 to 16 will remove more than 90% of all particles that are 0.3-1 µm in diameter, which includes the majority of bacteria.43

4. Ultraviolet Germicidal Irradiation

In a double-blind, multiple crossover study of office buildings, the use of ultraviolet germicidal irradiation (UVGI) effectively destroyed 99% of the microbial contaminants on irradiated surfaces in the ventilation system.63 In the study, airborne bacteria levels were lowered by 25% to 30%, and study participants reported reduced work-related respiratory and mucosal symptoms when UVGI was used.63

2. Viruses

Viruses, like airborne bacteria, can spread via aerosolization.64 Once inhaled, viruses can lead to infections such as the common cold, influenza, mumps, and varicella, among other illnesses. Viruses are generally less than 0.1 µm in size but are often found in suspended water droplets that are up to five µm in size, meaning that viruses can sometimes be removed with media filters. However, if they are aerosolized, filtration is more difficult.64

Between 1976 and 2006, influenza and influenza-related respiratory illness were responsible for 3,000 to 49,000 annual deaths in the U.S. alone. Currently, 5% and 20% of Americans contract the flu each year.65 Children, the elderly, pregnant women, and those with weakened immune systems are especially susceptible to influenza.66

Health Effects

Respiratory System

Influenza. Influenza, or the flu, is an acute, contagious viral infection. It is caused by a variety of mutations of the influenza virus and typified by an inflammation of the respiratory tract, resulting in fever, chills, muscular pain, and fatigue.65 Infected individuals can spread viral particles, which become aerosolized when a person coughs, sneezes, speaks, or merely breathes.65

Asthma. Inhalation of airborne viruses is a known trigger for acute asthma symptoms and may increase the risk of developing chronic asthma, especially in young children.67

Immune and Integumentary Systems

Varicella (chickenpox). Varicella, often referred to as chickenpox, is a common and incredibly infectious viral disease that affects both children and adults.68 The virus responsible causes both varicella and shingles. Varicella results in an itchy, blistery rash that lasts about a week and at times involves a fever or other symptoms. It is spread through the air when an infected person coughs or sneezes.68 Shingles is an outbreak of blisters or rashlike plaques on the skin marked by a painful, tingling, burning sensation and can last up to five weeks.69 Once a person has had varicella, they are at risk of developing shingles later in life.69

Immune and Digestive Systems

Mumps. Mumps is a viral disease that causes painful swelling of the saliva-producing glands in the mouth. There is no specific treatment for ridding the body of the disease, and treatments instead focus on controlling the symptoms with pain-relieving medication.70 Mumps is transmitted via saliva or mucus droplets when an infected person talks, coughs, or sneezes.71

Nervous System

Cognitive disorders. Exposure to the influenza virus during pregnancy may increase an infant’s risk of later developing bipolar disorder by four-fold and schizophrenia by three-fold, which may result from the activation of genes that increase the susceptibility for these disorders.72

Solutions

1. Ultraviolet Germicidal Irradiation

Because of their small size, viral particles, are difficult to filter out of the air. However, ultraviolet germicidal irradiation has been shown to kill or inactivate a range of airborne viruses thorough sterilization and it can limit their prevalence in ambient air and on surfaces.73 74

2. Media Filtration

Filters with MERV ratings of 17 or higher will remove at least 99.97% of all particles that are less than 0.3 µm in diameter, which can include viruses in airborne form.43

3. Fungi (Mold)

In the natural environment (outdoors), mold is essential for breaking down dead plant material. However, it may become a health hazard in indoor environments.75 Mold will grow anywhere that moisture and a food source are present, including on any organic matter, wooden wall studs or sheetrock.75 Mold reproduces by releasing tiny spores into the air. Therefore, if mold is present near an air intake duct, it can get inside and circulate throughout a building.

To date, there is no standard method for the detection and analysis of indoor mold, making interpretation of test results highly variable. An assessment of airborne concentrations of pathogenic fungal microorganisms is troublesome and can be inaccurate and misleading, as some pathogenic microorganisms may be hazardous at very low levels, while others may only become hazardous at high levels. Also, while some mold spores are resilient, others may become inert during handling and sampling, thereby distorting the findings.

In non-culture-based methods, such as microscopy and flow cytometry, microorganisms are identified and quantified regardless of whether they are dormant or deceased.76 The sampling time can vary over a wide range, yet the results can be quickly available. However, these results do not provide information about the possible toxic or allergic components related to the detected microorganisms. Furthermore, the procedures are time intensive and expensive. Analyses that detect the DNA, RNA, or specific proteins in molds or bacteria (e.g., polymerase chain reaction or immunoassays such as the Western blot) can be used to detect and identify non-culturable fungal species, while biomarkers for specific fungal biomass (essentially, fungal metabolites) can be used to measure and estimate actual fungal exposure.76

The EPA and the U.S. Department of Housing and Urban Development developed the Environmental Relative Moldiness Index (ERMI) as a metric for assessing relative indoor air quality in the American Healthy Homes Survey.77 ERMI analyzes dust collected from buildings for mold species and ranks it for potential risk and associated health effects (Figure 4).77

FIGURE 4: MOLDINESS INDEX IN U.S. HOMES.77
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Health Effects

Respiratory and Immune Systems

Asthma. The AAFA and the EPA note that inhaling the spores of mold and mildew can trigger an asthma attack in individuals who are sensitive to molds.78 79

Allergies. The AAFA notes that inhaling the spores of mold and mildew exacerbates allergies in susceptible individuals.78 The symptoms of mold allergies include congestion, dry and scaling skin, itching, nasal discharge, and sneezing. Individuals who are allergic to pet dander or pollen are more likely also to be allergic to fungi.78

Hypersensitivity pneumonitis. Hypersensitivity pneumonitis is a lung disease that can result from the inhalation of mold particles.80 The ALA notes that the inhalation of mold spores causes inflammation of the lung and respiratory tract tissues.80

The onset of hypersensitivity pneumonitis in indoor settings has been linked to air-conditioning units and humidifiers contaminated with bacteria and molds.81 Fungi that produce hypersensitivity pneumonitis include Aspergillus, a mold that is dangerous whether inhaled or ingested. Stachybotrys, known as “black” or “toxic” mold, and Penicillium are also known to cause hypersensitivity pneumonitis through the emission of mycotoxins.81

Respiratory System

Impaired respiratory function. Biological aerosols such as mold may cause impaired respiratory function.82 A study that administered questionnaires to nearly 15,000 parents or guardians of children found that the prevalence of all respiratory symptoms was consistently higher in children who lived in interior spaces with reported molds or dampness.82 Additionally, research with 269 healthy, non-asthmatic adults found an association between indoor mold exposure and reduced lung function, especially among female participants.83

Bronchopulmonary aspergillosis. Bronchopulmonary aspergillosis is a fungus-induced disease that is primarily found in the respiratory tract.84 85 The AAFA notes that the spores of mold and mildew can cause bronchopulmonary aspergillosis in individuals who are sensitive to mold.78

Allergic fungal sinusitis. A 2000 study notes that inhaling fungal spores can cause allergic fungal sinusitis in susceptible individuals. Some of the symptoms include nasal polyps, rhinosinusitis, and occasionally proptosis.85 Additionally, a 2016 review exploring the health effects of fungi exposure on humans indicated the relationship between indoor fungal exposure and the development of allergic fungal sinusitis in individuals with weakened ability to respond to the presence of fungi.86

Humidifier fever. Humidifier fever is a form of sick building syndrome that can be caused by mold spores in the humidifier system.60 It includes flulike symptoms such as fever, headache, chills, malaise, cough, and tightness in the chest. It usually occurs a few hours after exposure and is often due to the fungi found in humidifier reservoirs.60

Nervous System

Headaches. The EPA notes that when there is mold growing indoors, one of the more common reaction symptoms is a headache.87

Diminished neurobehavioral parameters. Studies investigating the effects of mold exposure on neurobehavioral function have found that those exposed to mold experience decreased function in regards to balance, reaction time, blink-reflex latency, color discrimination, visual fields, and grip.88 89 Notably, individuals with mold/mycotoxin exposures experienced similar neurobehavioral impairments as those who experienced adverse reactions to various chemical exposures.89

Solutions

1. Media Filtration

Filters with MERV ratings of seven or higher will remove at least 50% of all particles that are 3–10 µm in diameter, which includes mold spores.43

2. Source Control

Any reservoirs used for the containment of water that will be aerosolized (e.g., a humidifier) should be cleaned and properly dried between uses to prevent bacterial growth.62

3. Ultraviolet Germicidal Irradiation

UVGI and ultraviolet emitters can destroy airborne mold spores and stop fungal growth through sterilization.90 In a double-blind, multiple crossover study of office buildings, the use of ultraviolet germicidal irradiation (UVGI) effectively destroyed 99% of the microbial contaminants (including mold) on irradiated surfaces in the ventilation system. Study participants reported reduced work-related respiratory and mucosal symptoms when UVGI was used.63 Additionally, a case study of UVGI efficacy in a classroom setting found that compared to the control group, the UVGI classroom experienced significant reduction in total bacterial concentration in three of the four sampling months, indicating the potential for this technique in schools and other buildings.91

4. Dehumidification

The EPA notes that controlling indoor humidity can prevent the establishment and growth of mold.92 The agency recommends keeping indoor humidity levels below 60%, and ideally between 30% and 50%.92 Dehumidification is also recommended by the ATSDR to improve air quality and reduce the potential buildup of airborne allergens.51

Particulate Matter

Particulate matter air pollution is a complex mixture of small solid particles and liquid droplets in the air. Inhaling elevated levels of particulate matter have been shown to lead to various adverse health effects.93

Particulate matter can contain elemental and organic carbon, salts, mineral and metal dust, ammonia, and water, which coagulate together into tiny solids and globules.94 Both human-made (anthropogenic) and natural sources emit particulate matter or gaseous components that react in the air to form particulate matter. Particulates vary in size, shape, density, and chemical composition and are distinguished by aerodynamic diameter. Those designated as inhalable coarse particles have diameters larger than 2.5 µm and smaller than 10 µm (known as PM10), while fine particles have diameters of 2.5 micrometers and smaller (known as PM2.5). Ultrafine particles (UFPs) are of nanoscale and have diameters smaller than 0.1 µm (≤ 100 nanometers).94 Fine particles are more easily measured than ultrafine and form the basis for many air quality recommendations due to their significant health impacts.

FIGURE 5: EXAMPLES OF COMMON PARTICLE SIZES.95
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The size of particulate matter largely determines where in the respiratory system the particles are deposited (Figure 6).94 Because of the filtration provided by the nasal-pharyngeal and tracheobronchial regions, inhaled particulate pollution concentration is somewhat diminished by the time a particle reaches the deepest region of the lungs. The filtration provided by the body is more efficiently geared toward particles in the coarse particle range. Although ultrafine particles are not considered any more or less toxic than larger particles, concern arises from the more significant number of particles needed to create a similar mass concentration, thereby increasing the potential for damage or adverse effects.94

FIGURE 6: LOCATION OF PARTICLE INTERACTION WITHIN THE AIRWAY.96
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1. Coarse Particulate Matter (PM10)

Coarse particulate matter, known as PM10, refers to particles 10 µm in diameter or smaller.94 Due to the relatively larger size of the particles, PM10 is generally trapped in the head and upper airway region of the body and does not penetrate as deeply into the lungs as fine (PM2.5) or ultrafine particulates, which is why they are less of a health concern.94 Nevertheless, coarse particles have been associated with negative health effects. A study investigating the effects of Saharan dust on daily mortality rates in Barcelona found an 8.4% increase in mortality with a 10 µg/m³ increase in PM10. The simultaneous increase in PM2.5 did not lead to an increased mortality on Sahara-dust days.97 A study across 112 U.S. cities, analyzing the effects of particulate matter on mortality found a stronger than expected association between coarse particles and death.98 The study suggested that regional differences in the toxicity of coarse particles and the observed effects on health varied by area and did not necessarily follow the same pattern of variance as PM2.5.98 This point was expanded upon more recently in laboratory research that showed that PM10 is likely to generate a more generic symptomatic effect, while the smaller PM2.5 is likely to be more reactive at the cellular level.99

When a particle is not formed by secondary gases, its size is directly attributable to the amount of energy used to generate it, i.e., the more energy used, the smaller the particle created.64 When particles are mechanically generated from construction, agricultural, road traffic, volcanic and other sources, they tend to be larger (closer to 10 µm in diameter or more) and fall into the coarse (PM10) category. When the National Ambient Air Quality Standards (NAAQS) were established in 1971, the Total Suspended Particulates (TSP) limit was set at 260 µg/m³ on average over a 24-hour period (not to be exceeded more than once per year) and at 75 µg/m³ on average over a year. In 1987, PM10 replaced TSP as the standard of measurement, and the 24-hour value was set to 150 µg/m³, which is not to be exceeded more than once per year, on average over a three-year period. The annual limit for PM10 was removed as of 2006.100 The WHO’s expanded guidelines for PM10 from 2005 recommend a stricter limitation of 50 µg/m³ for a 24-hour period and 20 µg/m³ for a year.101 The U.S. Occupational Safety and Health Administration (OSHA) recommends a time-weighted average for respirable particles not to exceed 5,000 ppm during any eight-hour work shift of a 40-hour workweek.102

Health Effects

Respiratory System

Asthma. A bidirectional case-crossover and time-series analysis found a 14% to 18% increase in asthma hospitalizations among 6-12-year-old children in Toronto between 1981 and 1993 during increased exposure to PM10, an increment of 8.4 µg/m³ over an average of six days. The effects remained after adjusting for specific gaseous pollutants (NO2, CO, SO2, O3) as well as for PM2.5.103 Additionally, exposure to PM10 may influence the risk of asthma development. A systematic review and meta-analysis of 41 studies exploring the relationship between exposure to traffic-related air pollution and asthma found a significant association between exposure to PM10 and risk of developing childhood asthma.104

Respiratory mortality. A study analyzing data from 112 U.S. cities found an increase in respiratory mortality by up to 1.68% and a 0.98% rise in all-cause mortality (which varied by climate zone) associated with increased levels of particulate matter.98 The findings made the distinction between coarse and fine particles with the coarse particle findings being higher than previously thought.98 A study exploring the health effects of air pollution in Europe and North America found that among cities with available air pollution data, the combined effect of PM10 on all-cause mortality across all ages ranged from 0.2% to 0.6% for a 10-µg/m³ increase in ambient PM10 concentration.105

Cardiovascular System

Decreased heart rate variability. Heart rate variability (HRV) is a measure of cardiac autonomic balance, and decreased levels of HRV are associated with an increased risk of cardiac mortality.106 A study involving 19 nonsmoking patients with known coronary artery disease living in California’s Coachella Valley, a desert region with high PM10 values, found an association between HRV and PM10 levels. The observed HRV values, including time-domain, geometrical and frequency-domain HRV variables, suggested a close, timely effect between PM10 exposure and decrease in HRV.106

Another study found similar decreases in HRV variables associated with a 1 µg/m³ increase in PM10 in asthmatic patients over a 12-week period.107 While clear changes were observed in HRV, no diminishment in respiratory function was found to be associated with fine PM2.5.107

Coronary heart disease. A cohort-study followed 3,239 adults for 22 years, measuring monthly levels of air pollutants and asking subjects to fill out and update lifestyle questionnaires.108 Using a single-pollutant model, the risk for fatal coronary artery disease in women was 38% higher with every 10 µg/m³ increase in PM10. No similar association was found in males, however.108 It has been found that the elderly and immunocompromised are more likely to suffer a cardiac event associated with PM10 exposure.109

Solutions

1. Media Filtration

Filters with MERV ratings of eight or higher will remove at least 70% of all particles that are 3–10 µm in diameter, and those with a rating of 12 or higher will remove at least 90%.43

2. Source Reduction

By eliminating particulate matter generators, such as tobacco smoke and indoor combustion of biofuels, and by ensuring that all ventilation systems are in proper working order, the amount of particulate matter indoors can be greatly reduced.110 Additionally, the removal of permanent carpets prevents re-entrainment of particles during cleaning.110

3. Entryway Walk-Off System

Walk-off mats are a useful and simple means of preventing particulate matter from being carried indoors on the soles of shoes.

4. Kitchen Exhaust Hoods

One method of indoor PM production is by high-temperature stovetop cooking. Properly venting hoods can greatly reduce production of this pollutant.111

5. Vehicle Idling Limits

Cars use more fuel and cause more engine wear when they idle for more than 30 seconds compared with turning off and restarting the engine.112 Heavy-duty diesel vehicles generate approximately 20,000 µg of PM10 per minute of idling.113

2. Fine Particulate Matter (PM2.5)

Particles with a diameter less than 2.5 µm are known as PM2.5, and are referred to as “fine” particles. These particles are believed to pose the greatest risk to human health.114 Fine particles primarily form from combustion processes such as coal burning, diesel emissions, gasoline combustion, power generation and other industrial processes. Additionally, some transformation products, such as sulfate and nitrate particles or secondary organic aerosols from volatile organic compound emissions, are counted as fine particles.

Figure 7 illustrates the distribution of PM2.5 air pollution worldwide in 2010. Desert areas have some of the highest concentrations of PM2.5. Large areas of rapidly industrializing countries are also subject to this type of pollution.115

Figure 7: Global distribution of PM2.5 pollution (Average from 2001-2006).115
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In a landmark Harvard Medical School study analyzing PM2.5 levels from six U.S. cities between 1979 and 1988 and in the subsequent follow-up analyses, increased PM2.5 levels from mobile combustion sources (traffic) and coal combustion sources were associated with increased daily mortality rates.116 117 Another large Harvard study conducted from 2000 to 2007 found that a 10 µg/m³ reduction in the concentration of PM2.5 was associated with an average 0.35-year increase in life expectancy in 545 U.S. counties, after controlling for demographic and socioeconomic characteristics and smoking prevalence.118 The New York City Department of Health estimates that each year in the city, PM2.5 pollution causes more than 3,000 premature deaths and more than 8,000 hospital admissions.119

The WHO indicates that the risk for various health issues has been shown to increase with exposure to PM2.5, and there seems to be no exposure threshold level at which health effects can be considered negligible.101 Therefore, it set limits for PM2.5 in 2005 of 25 µg/m³ for a 24-hour average period and 10 µg/m³ on average for a year (Figure 8).101

The EPA did not regulate PM2.5 under NAAQS until 1997 when it set limits of 65 µg/m³ averaged over a 24-hour period and 15 µg/m³ averaged over a year.100 In 2006, the agency reduced the 24-hour average to 35 µg/m³, and in 2012 it reduced the annual average to 12 µg/m³ (Figure 8). Annual standards are averaged over three years, which tends to reduce the measured impact of short-term air quality events such as forest fires.100

FIGURE 8: CHANGING AIR QUALITY STANDARDS FOR PARTICULATE MATTER.100 101
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Health Effects

Respiratory System

Respiratory irritation. The EPA reports that PM2.5 causes short-term respiratory irritation, including eye, nose, throat and lung irritation, coughing, sneezing, runny nose, and shortness of breath.120 Additionally, PM2.5 has been shown to have a deleterious effect on respiration, with statistically significant increases in hospital admissions attributed to elevated levels of PM2.5 pollution.121

Lung cancer. A study of 1.2 million adults by the American Cancer Society analyzed the relationship between air pollution, vital status, and cause of death, and demonstrated that every 10 µg/m³ increase in fine particulate matter could be associated with an approximately 8% increase in the risk of lung cancer mortality.122

Respiratory-related infant mortality. A study analyzing post-neonatal deaths within five miles of a measuring station in California in 1999–2000 found an increased odds ratio of 2.13 in post-neonatal deaths from respiratory causes with each 10 µg/m³ increase in PM2.5.123 A study evaluating the effect of acute exposure to particulate matter on infant mortality in Tokyo, Japan from 2002-2013 found a significant mortality risk due to exposure to PM2.5, with an odds ratio of 1.06 for infant mortality and 1.10 for postneonatal mortality with a 10 µg/m³ increase in PM2.5.124 Notably, adverse health effects were observed even when PM2.5 levels were below Japanese air quality guidelines.124

Cardiovascular System

Cardiopulmonary diseases. An analysis concluded that every 10 µg/m³ increase in fine particulate matter could be associated with approximately a 6% increase in the risk of cardiopulmonary mortality.122 In addition to chronic cardiac effects associated with PM2.5, evidence shows changes in heart rate immediately following exposure, thus increasing the risk of an acute cardiac event in people with preexisting conditions.125

Atherosclerosis. A cross-sectional study with 798 patients investigated the association between subclinical atherosclerosis (using carotid intima-media thickness [CIMT]) and long-term exposure to PM2.5.126 The study found that the CIMT increased by 3.9% to 4.3% with a PM2.5 exposure of 10 µg/m³. This was the first epidemiological association between air pollution and atherosclerosis.126 The Multi-Ethnic Study of Atherosclerosis and Air Pollution, a prospective 10-year cohort study of 6795 individuals aged 45-84, furthers this evidence. Findings indicate that exposure to increased concentrations of PM2.5 was associated with progression of coronary calcification, an indication of disease acceleration.127

Solutions

1. Vehicle Idling Limits

Cars use more fuel and cause more engine wear when they idle for more than 30 seconds compared with turning off and restarting the engine.112 Heavy-duty diesel vehicles generate approximately 18,000 µg of PM2.5 per minute of idling.113 By limiting vehicle idling on nearby roads and driveways, buildings can reduce a local source of particulate matter pollution.

2. Source Reduction

In some cities and other areas, residual fuel oil, a heavier oil, is a common fuel used to provide heat and hot water in buildings. Evidence shows that fuel oil quality and type of heating system play a major role in air quality and the health of individuals living within a building and surrounding areas.128 The consumer does often not make these choices, but local governments can regulate them.

3. Cleaner Combustion Sources

Globally, wood stoves and biomass burning are used as a primary method of heating, and it has been shown that they can have a dramatic effect on local air quality.129 For example, in Libby, Montana, 80% of ambient PM2.5 levels were attributable to residential wood stoves. After 95% of stoves in the community were replaced with EPA-certified lower emission stoves, the average PM2.5 levels in the winter dropped by 27%. However, not all exchange programs are as successful.129

4. Media Filtration

Filters with MERV ratings of 10 or higher will remove at least 50% of all particles of 1–3 µm, and those of 13 or higher will remove at least 90%.43 A MERV 14 filter will remove at least 75% to 85% of particles of 0.3 to 1 µm.43

5. Entryway Walk-Off Syste

Walk-off mats are a useful and simple means of preventing particulate matter from being carried indoors on the soles of shoes.

6. Kitchen Exhaust Hoods

One method of indoor PM production is by high-temperature stovetop cooking. Proper venting hoods can significantly reduce production of this pollutant.111

3. Ultrafine Particles (UFPs)

Ultrafine particles are very small particles with diameters of less than 0.1 µm (100 nanometers) and are also referred to as PM0.1 or nanoparticles. They are difficult to characterize, as air concentrations are highly dependent on the proximity to sources such as high-volume traffic. Unlike PM10 and PM2.5, UFPs are typically measured using particle counts per unit of volume (e.g., ppm) rather than mass per unit of volume (e.g., 10 µm/m³). They have a much higher count-to-mass ratio and consequently a nearly negligible mass compared with larger airborne particles. Their small size means it is possible though not always likely for them to be drawn deep into the lungs, maximizing their damage (Figure 10). UFPs are currently unregulated and have high spatial and temporal variability.130

UFPs are responsible for some of the health effects caused by PM2.5 and PM10 due to the fact they often make up a portion of the particulate mix.131 Generally, exposure to UFPs is generally not a homogenous event, and the toxic effects of UFPs can be significantly enhanced by the presence of other pollutants as well as small differences in chemistry, size, and solubility.132

Health Effects

Respiratory System

Respiratory inflammation. A 2003 study comparing the ability of coarse, fine, and ultrafine particles to cause oxidative stress, a precursor to pulmonary inflammation, found that UFPs demonstrated increased biological potency by inducing structural damage in the mitochondrial region.133 Additionally, their chemical composition included a high amount of reactive oxygen species, a further indication that UFPs induce oxidative stress.133

Peak expiratory flow. A study evaluating the effects of a particulate matter mix on a group of nonsmoking, asthmatic adults found a greater decrease in the subjects’ peak expiratory flow when the portion of UFPs in the mix was larger.134 The authors concluded that respiratory effects are positively associated with the number of ultrafine particles in ambient air.134 Additionally, a 2008 study of cyclists with short-term exposure to UFP’s found significant associations between increased levels of UFP concentrations and reduced lung function.135

Heart Disease. An analysis of more than 100,000 teachers in the state of California over the course of six years showed that not only is exposure to UFP significantly associated with ischemic heart disease (IHD) but that it is highly dependent upon the elemental makeup of the UFPs.136 The study showed that the fraction of UFPs with the greatest association to IHD comes from mobile source emissions (e.g., diesel and gasoline).136

Solutions

1. Kitchen Exhaust Hoods

One method of indoor PM production is by high-temperature stovetop cooking. Proper venting hoods can greatly reduce production of this pollutant.111

2. Vehicle Idling Limits

Cars use more fuel and cause more engine wear when they idle for more than 30 seconds compared with turning off and restarting.112 Since vehicle emissions are the major source of ultrafine particles in most cities, limiting idling near buildings can help reduce local concentrations.130

Specific Airborne Particles and Fibers

The presence of tiny solid particles in inhaled air is often sufficient to cause damage to the respiratory and circulatory systems. However, particulate matter becomes inherently more dangerous with the presence of chemicals such as diesel exhaust, lead, mercury, or asbestos.

1. Diesel Exhaust Particulate Matter

Due to incomplete combustion processes, the exhaust of diesel engines contains various gases, liquids, and solid particles composed of elemental carbon with sulfates, metals, and other substances.137 Diesel exhaust particulate matter (DEP) created by trucks, boats, farm equipment, and generators can cause adverse health effects, such as coughing and nausea (especially in children) and short-term irritation of the eyes and throat.137

Some of the pollutants associated with diesel exhaust, specifically sulfur oxides, are becoming less of a concern as diesel fuel is becoming cleaner. The EPA’s 2006–2010 phase-in for ultralow sulfur diesel fuel is estimated to decrease exhaust emissions by 90%.138

Although DEP is not directly part of NAAQS, some of the constituents of DEP are. The EPA recommends an outdoor diesel exhaust concentration, which includes DEP, of less than 5 µg/m³ (one-third of the NAAQS PM2.5 limit), which is set as a reference concentration intended to protect against non-carcinogenic health effects.137

Health Effects

Respiratory System

Allergic sensitization. In a study of ragweed-sensitive subjects, diesel particulates were shown to potentiate the production of immunoglobulin-E (IgE), a class of antibodies known to play a crucial role in hypersensitivity 139. This correlation suggests that diesel particulate matter increases sensitization to allergens.139

Allergic asthma. In an allergy challenge study researching the effects of DEP on allergic asthma, researchers exposed mice to 100 µg of DEP intratracheally for six weeks, as well as to an antigen (ovalbumin), or to a vehicle only or an antigen only. The antigen-induced accelerated airway inflammation and increased the number of goblet cells in airways and the local expression of Th2 cytokines in the mice also exposed to DEP. The authors concluded, “These results provide the first experimental evidence that DEP can enhance the manifestations of allergic asthma”.140 Additionally, research on inner-city children shows that when pollution elements are individually assessed, it is the carbonaceous soot from diesel exhaust that is most highly correlated with the exacerbation of existing asthma.141

Immune function. In a study on the effects of DEP on immune function, researchers exposed rats to extremely high levels of DEP, either 50 or 100 mg/m³, or to purified air (exposure to this level of DEP is unlikely for humans in normal settings).142 Two hours after the exposure, the rats were exposed to the bacterium Listeria monocytogenes. The researchers found that in rats exposed to DEP, phagocytosis and Listeria-induced basal secretion of interleukin-1β (IL-1β) and IL-12 by alveolar macrophages was suppressed in a dose-dependent manner. The authors concluded that DEP retards bacterial clearance from the lungs, weakens innate immunity and may suppress cell-mediated immunity, thus increasing the susceptibility to bacterial infection.142 Additionally, a study exploring the impact of exposure to DEP extracts on human macrophages (key players in the human immune response) found that DEP exposure may alter expression of certain essential macrophage functions, potentially resulting in deleterious immune effects.143

Respiratory and Endocrine Systems

Lung Cancer. In 2012, WHO’s International Agency for Research on Cancer (IARC) classified diesel exhaust as a known (Group 1) human carcinogen.144 In an effort to further explore the mechanisms of carcinogenicity, an analysis from the Health Effects Institute (HEI), concluded that “the small respirable soot particles in diesel exhaust are primarily responsible for lung cancer developing in rats exposed to high concentrations of diesel emissions”.145 However, more research is needed regarding the mechanisms and the particle concentrations and duration of exposure that lead to lung cancer and before these findings can be extrapolated to humans.145

Solutions

1. Vehicle Idling Limits

Avoiding motor vehicle idling, including cars with diesel engines, can minimize the risk of diesel exhaust particles.137

2. Media Filtration

Diesel exhaust particulates are composed of fine (PM2.5) and ultrafine (PM0.1) particulate matter.137 Filters with MERV ratings of 10 or higher will remove at least 50% of all particles of one to three µm, and those of 13 or higher will remove at least 90%. A MERV 14 filter will remove at least 75% to 85% of particles of 0.3 to 1 µm.43

2. Lead Particulates

Lead is a corrosion-resistant, dense and malleable blue-grey 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, gutter joints, and roof parapets. Until it was banned in 1977, lead-based paint was commonly used in homes and other buildings. Lead pipes were used for connecting buildings to water mains and declined in use after 1930.146 Existing lead in the environment is an ongoing health issue.147 Mining, smelting, and refining activities also result in significantly increased levels of lead in the environment.147

Lead is a potent toxicant that can affect most systems and organs in the body.148 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.148

Lead becomes inhalable once it is burned or melted and released as a fume, and this route of exposure generally affects occupational workers. Lead may also be inhaled when dust that contains lead becomes airborne. Airborne lead particles in outdoor air can also be tracked into the indoor environment through foot traffic or as dust.12 In response to the hazards and pervasive nature of lead, the original NAAQS limit for lead, 1.5 µg/m³, was reduced by the EPA in 2008 to 0.15 µg/m³ for a rolling three-month average.100 The CDC and OSHA have also set an eight-hour average indoor air maximum concentration for lead at 50 µg/m³. Despite such efforts, as recently as 2011, the CDC confirmed that as many as 535,000 children have high lead blood levels.149 150

Lead was used in gasoline in the U.S. until 1988 (except for Alaska, where it was used until 1991) and was officially banned from use in gasoline in 1995.151 Apart from exposure through food, water, and soil, atmospheric lead is a major source of pollution. Exposure to airborne lead can occur through inhalation of combustion products, including waste, coal, oil, and tobacco, as well as emissions from metal manufacturing and lead smelting.

The phase-out of leaded gasoline has however greatly reduced ambient lead levels. Between 1980 and 2007, average ambient concentrations in the U.S. decreased by almost 94%.152 In 2002, average ambient lead concentrations were less than 0.05 µg/m³.153

Communities living near smelting sites are especially at risk to high blood lead levels. A study measuring blood levels in 781 children living near a lead smelter in northern Idaho concluded that ambient air lead exposure was the strongest individual factor that influenced lead blood levels, and it explained 55% of the occurring variances in lead blood levels.154

For more on the effects of lead and ways to avoid exposure, refer to the Water WELLography™ and Materials WELLography™.

Health Effects

Nervous System

Health Hazard. Although lead accumulates in bone marrow, the nervous system is the main target for toxicity. In 2001, the Missouri Department of Health and Senior Services and the Jefferson County Health Department conducted blood lead screening of a community in Herculaneum, Missouri, near a lead-processing plant.155 The 52-acre facility, an active processing plant that smelts lead ore (80% lead sulfide), sits adjacent to residential neighborhoods to the north, south, and west. 935 people were screened, of which 655 were adults aged 18 or older. Results indicated that 28% of children in the community had lead poisoning, or had blood levels known to cause harmful health effects, at 10 µg/dL or higher. Given the known effects associated with lead levels of 10 µg/dL, the CDC has lowered the reference level of lead in blood for children to 5 µg/dL.155 The average blood lead level in young American children, according to data from the National Health and Nutrition Examination Survey (NHANES), conducted by the CDC between 1996 and 1999, is 2 µg/dL.156

Impaired cognitive development. Children under the age of seven are especially at risk for exposure, as even low blood levels can result in a deficit in cognitive development.157 There is no known safe level of lead exposure for children. Exposure often causes no obvious symptoms but has been linked to loss of cognition, shortened attention span, altered behavior, dyslexia, attention deficit disorder.158 Research suggests a neuropsychological manifestation due to low-doses exposure during childhood affects the function of a child’s central nervous system, even after the ingestion of lead has declined or stopped.159 Furthermore, lead exposure is cumulative. Thus, low levels can cause cognitive decline if the exposure takes place over long periods of time.160

Solutions

1. Pollutant Restriction and Abatement

All surface materials in buildings should contain no more than 100 ppm by weight of added lead. For buildings constructed before 1978, lead evaluation and abatement should be done in accordance with the EPA guidelines.161

2. Air Filters

Air filters with MERV ratings of 10 or higher will remove at least 50% of all particles of one to three µm, filters at MERV 13 or higher will remove at least 90% of particulates along the same range.43 A MERV 14 filter will remove at least 75% to 85% of particles 0.3 to one µm.43

3. Mercury Particles

Mercury exists in three forms: elemental, inorganic, and organic. All forms are toxic, although to different extents and with different effects.162 It is released into the air when wood, coal, gas, or waste containing mercury is burned and can move far from its initial source through the atmosphere.

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.163 Inorganic mercury was mostly used in the past in skin-lightening creams and soaps and 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.164 165 166 The majority of emissions of mercury are from the combustion of fossil fuels and waste.167 While agricultural and pharmaceutical uses of inorganic mercury have mostly ceased in the U.S., mercuric chloride is still used as a disinfectant and pesticide.

For more information on mercury, refer to the Materials WELLography™.

Health Effects

Urinary System

Kidney disease. The WHO reports that inhalation of mercury vapor may produce harmful effects on the kidneys, including increased protein in the urine and kidney failure.168 More specifically, a study in Runcorn, England, which had been the site of high industrial activity for more than 100 years, found a significant exposure-response relation between modeled estimates of mercury exposure and risk of death from kidney disease.169 The authors suggested that long-term, low-level exposure to the mercury-bearing exhausts of the nearby chlor-alkali process plant and coal-fired power station may be associated with excess kidney disease mortality in the population.169

Nervous System

Developmental disabilities. A comparison of administrative data from the Texas Education Agency and data regarding environmentally released mercury from the EPA’s Toxics Release Inventory found an association between environmentally released mercury and developmental disabilities at a county level mercury.170 On average, the rate of special education services increased by 43% and the rate of autism increased by 61% for every 1,000 pounds of environmentally released mercury.170 Inhalation of mercury vapor among children is also associated with disturbances in the central nervous system, such as tremor and coordination difficulties, as well as mercurial erethism, which includes symptoms such as excitability, loss of memory, insomnia, and extreme shyness.171

Solutions

1. Media Filtration

Atmospheric particulate mercury tends to be between one and six µm in diameter.172 Filters with MERV ratings of 10 or higher will remove at least 50% of all particles of one to three µm, and those of 13 or higher will remove at least 90%. Filters with MERV ratings of eight or higher will remove at least 70% of all particles of three to 10 µm, and those of 12 or higher will remove at least 90%.43

4. Asbestos Fibers

A naturally occurring mineral comprised mostly of fibrous silica, asbestos has been mined and used for thousands of years.173 It is malleable and chemically inert, has high electrical and thermal resistance, and has been used in insulation, as a fireproofing material, in automobile brakes, and in many other products.

The U.S. has phased out most uses of asbestos,173 whereas the European Union forbids the manufacture or import of any products that contain asbestos.174

When asbestos-bearing sheetrock or building materials are disturbed during a renovation, asbestos fibers are released into the air.173 The most common pathway into the human body is through inhalation. Inhaled asbestos fibers can lead to lung cancer and lung scarring. The fibers can become lodged in the lungs and over the course of several years scar the lungs, resulting in chronic coughing and shortness of breath. This condition, known as asbestosis, is untreatable. As with radon exposure, the risk is compounded for individuals who smoke.173 Workplace exposure to asbestos is also linked to cancer of the larynx, ovaries, and other organs.173

Detailed health effects, as well as solutions on how to prevent exposure to asbestos, are included in the Materials WELLography™.

Gases

There are a wide variety of potentially toxic gases present throughout our environment, which come from multiple sources. Below are some of the most commonly encountered gases.

1. Cardion Dioxide

Most living organisms, including humans, exhale CO2 through respiration.175 Without sufficient ventilation, CO2 would continuously accumulate in occupied buildings. It is easy to detect, so it is often used as an indicator of occupancy when monitoring and adjusting ventilation systems. Although it is not harmful at commonly experienced concentrations, high CO2 levels may be linked to the presence of odors and other volatile organic compounds from improperly tuned ventilation systems.175

The EPA notes that indoor concentrations of 1,000 ppm (0.1%) for continuous exposure indoors are indicative of lack of proper ventilation 176 and the National Institute for Occupational Safety and Health (NIOSH) and OSHA recommend 5,000 ppm as an eight-hour time-weighted average.102 The Illinois Department of Public Health recommend floor-wide averages of 800 ppm or less.177

Health Effects

Nervous System

Impaired decision-making. New evidence suggests a link between CO2 exposure and impaired decision-making.178 A 2012 study exposed participants to three different CO2 levels in an otherwise unchanged office-like room for two and a half hours at a time and asked them to complete nine decision-making tests and questionnaires. Relative to the lowest level of CO2 exposure of 600 ppm, moderate but statistically significant reductions in performance were seen at 1,000 ppm. At 2,500 ppm, large statistically significant reductions in performance were observed (Figure 9). The authors suggested that CO2 may not only be an indicator of the presence of other air pollutants but by itself may affect the decision-making processes at levels considered not threatening to human health.178

Headaches. At 4,000 ppm, a level roughly 10 times that found in the atmosphere, carbondioxide can cause headaches.179

FIGURE 9: CARBON DIOXIDE LEVELS AND DECISION-MAKING.178
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Solutions

1. Adequate Ventilation Rates

ASHRAE recommends ventilation rates based on occupancy for a variety of spaces in its Standard 62.1, Ventilation for Acceptable Indoor Air Quality in Table 6.2.2.1.180 Exact rates differ by use type, but for most spaces with stationary activities, they range from five to 10 cfm/person, or 0.06 to 0.12 cfm/ft².180 Other standards also specify recommended ventilation rates in buildings, such as EN 15251, AS 1668.2, CIBSE Design Guide A, and others.

ASHRAE standards also allow buildings to vary their ventilation rates depending on changing occupancy levels. These demand-controlled ventilation systems can respond directly to CO2 levels, or to occupancy sensors or schedules.180

2. Operable Windows

Windows that can be opened by the people within the building or automated systems can rapidly increase the amount of outside air entering a building. While this is effective at reducing carbon dioxide levels, care must be taken to avoid introducing air that is high in other pollutants, such as ozone and particulate matter.110

2. Carbon Monoxide

Carbon Monoxide (CO) is a colorless, odorless, and tasteless gas that is slightly lighter than air. It results from the partial oxidation of carbon when there is not enough oxygen available to form CO2.181 CO also occurs in small quantities during normal animal metabolism. While carbon monoxide does not usually present a problem outside (except in high traffic or automobile tunnels), in indoor spaces with inadequate ventilation, the gas can accumulate more easily. Therefore, ventilation is important, especially in rooms that contain CO sources, such as garages, kitchens with gas stoves, and rooms with gas clothes dryers. Just two minutes of operating a car in a garage, even with the garage door open, can increase the CO level to 500 ppm, which is 55 times above the acceptable limit set in the EPA’s NAAQS.181

CO has 210 times the binding affinity to hemoglobin of O2, and therefore it blocks oxygen binding and prevents the oxygen from being carried throughout the body.182 The lack of O2 being delivered causes a condition known as hypoxia. Hypoxia can cause nausea, fatigue, and death. Pregnant women and smokers are at higher risk of severe health effects due to CO since they already have compromised O2 delivery mechanisms.182

FIGURE 10: HEMOGLOBIN AND GASEOUS EXCHANGE.182
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Every year in the U.S. unintentional CO poisoning (not linked to fires) results in 20,000 visits to the emergency room, more than 4,000 hospitalizations, and approximately 400 deaths.183 Carbon monoxide poisoning is associated with a variety of nonspecific symptoms. At levels twice the personal exposure limit (PEL) of 35 ppm some people may experience headaches, fatigue, and nausea.184 Between 10-40,000 Americans miss work or seek medical attention each year due to CO exposure,185 and 170 people die per year from CO poisoning in the U.S., excluding deaths related to automobile emissions.186

The EPA requires all U.S. localities to maintain outdoor CO concentration below a nine-ppm average for any eight-hour period and 35 ppm for any one-peak hour, and all counties currently adhere to this regulation.187 188 The WHO also recommends limiting exposure based on time: 90 ppm for 15 minutes and 10 ppm for an eight-hour exposure.189 For occupational safety, OSHA initially recommended 50 ppm as a transitional time-weighted average over eight hours, and NIOSH set the final recommendation at 35 ppm.190

Health Effects

Cardiovascular System

Cardiovascular disease mortality. A study analyzed the cardiovascular health of 5,529 tunnel officers employed by the Triborough Bridge and Tunnel Authority in New York City between 1952 and 1981, who were exposed to increased CO levels.191 CO measurements varied between 35 ppm and 300 ppm, with peaks during rush hour, until ventilation was increased in 1970. Compared to the New York City population, as well as to unexposed bridge officers with similar backgrounds and age, the tunnel officers had a 35% higher risk of arteriosclerotic heart disease mortality.191

A study of 19 European Union cities found a 1.25% increase in cardiovascular deaths associated with a 0.87 ppm (one mg/m³) increase in the two-day average CO levels.192

Nervous System

Delayed neuropsychological sequelae (DNS). DNS usually occurs some weeks after severe CO poisoning and involves a-specific symptoms, such as a variety of neurological deficits, including cognitive and affective problems. In a retrospective study examining medical records of all admitted CO-poisoned patients in the emergency department of Care University General Hospital in Florence, Italy, between 1992 and 2007, 24.1% of the 141 patients participating in the follow-ups were diagnosed with DNS a month after their initial release from the hospital.193 Similarly, a study of 100 patients experiencing acute CO poisoning found that 20% developed DNS, with poorer outcomes associated with older age as well as those who experienced earlier onset post-poisoning.194

Headache. The CDC notes that headaches are one of the most common symptoms of CO exposure.195 A study involving 100 patients who had been diagnosed with acute CO poisoning investigated the subjects’ headache symptoms in order to develop a better diagnostic protocol for CO poisoning. The headaches described varied—ranging from dull to sharp, continuous to intermittent, or throbbing, and no typical characteristic of a CO-induced headache could be defined.196

Solutions

1. Kitchen Exhaust Hoods

Carbon monoxide is an odorless colorless gas produced by space heaters, gas stovetops, and ovens. Venting hoods over the stove can greatly reduce this pollution.111

2. Vehicle Idling Limits

Cars use more fuel and cause more engine wear when they idle for more than 30 seconds compared with turning off and restarting the engine.112 Cars and trucks that use gas generate approximately 1.2 g CO per minute and heavy-duty diesel vehicles generate 0.43 g/min CO per minute of idling.113 By limiting vehicle idling on nearby roads and driveways, buildings can reduce a local source of particulate matter pollution.

3. Ozone

Ozone (O3) is a reactive oxygen molecule that can impact our health. According to the EPA, ozone can trigger a wide variety of effects, including chest pain, coughing, throat irritation, and congestion, and can worsen asthma, emphysema, and bronchitis.197

Ozone is most often formed by a reaction in the atmosphere between solar radiation (sunlight) and oxygen. It can also be generated indoors by copy machines, high voltage electronics, and specific ozone generators used in air purifications. Ground-level ozone, the type that affects humans, is created when pollutants from cars, power plants, boilers, chemical plants, and other sources react with sunlight.197 Ozone enters buildings through ventilation systems, particularly when ozone levels are high, like on hot sunny days.

The photochemical processes involved in the formation of ozone are relatively well documented and can be summed up as the chain reaction initiated by sunlight creating water vapor and singlet oxygen (O1) (Figure 11).198 Since singlet oxygen is not stable in the atmosphere, it quickly binds with available oxygen (O2) to form ozone (O3).

Ozone naturally occurs as a layer in the earth’s upper atmosphere (stratosphere) and provides a crucial service necessary for life on earth by filtering out ultraviolet light (radiation). Ozone generated at ground level is chemically the same as upper atmospheric ozone (O3). However, due to health effects associated with direct inhalation exposure, it is a negative air pollutant with no beneficial effect like its upper atmospheric counterpart.198

FIGURE 11: PHOTOCHEMICAL FORMATION OF OZONE.199
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The EPA recently reduced the limit on ambient outdoor ozone levels to 75 ppb from 80 ppb, averaged over eight hours (the EPA considers a region noncompliant if the fourth highest measurement of the year exceeds restriction).200 However, the Clean Air Scientific Advisory Committee (CASAC) of the EPA recommends setting a standard between 60 and 70 ppb and does not believe the 75-ppb limit to be sufficiently protective.200

OSHA guidelines in the workplace are based on time-weighted averages and are limited to 100 ppb for eight hours of exposure per day while doing light work.201 According to NIOSH, ozone levels of five ppm (5,000 ppb) or higher are considered immediately dangerous to life or health. The NIOSH recommended exposure limit for ozone, consistent with OSHA, is 100 ppb.201

Several hundred counties in the U.S. exceed the EPA’s limit of 75 ppb, with only a few rural counties measuring ozone levels of 60 ppb, and almost no region in the country meets WHO’s 51-ppb limit.202 If all locations in the U.S. could meet the new standard of 75 ppb, the EPA estimates that as many as 2,300 fewer deaths and 43,000 fewer lost workdays would be accumulated over the next half-decade. If the outdoor air standards were set at a more stringent level of 65 ppb, the EPA believes the cleaner air would prevent up to 7,100 deaths and 110,000 lost workdays.202

FIGURE 12: DEVELOPMENT OF OZONE STANDARDS.100 101
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Health Effects

Respiratory System

Respiratory diseases. Ozone found at ground level is highly toxic, and exposure can result in triggering asthmatic events and lung damage.203 204

A study in 16 Canadian cities counted a total of 720,519 hospital admissions due to respiratory diseases from 1981 to 1991.205 After controlling for covariates and other air pollutants (SO2, NO2, CO), the study found an association between ozone levels recorded one day before admission and the number of admissions (relative risks varying among cities between 1.0 and 1.088) from April to December. The authors suggest that relatively low ambient ozone levels lead to excess hospital admissions for respiratory diseases.205 Additional research has found that among healthy individuals there is no uniform response pattern, but airway responses, epithelium permeability, and forced expiratory volume were all significantly altered among different sub groups, indicating an array of possible negative outcomes.206

Respiratory mortality. A 2009 epidemiological study analyzed nearly half a million people living in almost 100 metropolitan statistical areas across the lower 48 states of the U.S.207 The authors found that increased concentrations of O3 corresponded to higher rates of respiratory mortality, independent of other pollutants. A 10 ppb increase in ambient levels was associated with a 4% increase in the risk of death.207

Respiratory System

Asthma. The EPA states that long-term exposure to ozone is not only linked to aggravation of pre-existing asthma, but it also likely one of the causes of asthma development.208 Children in particular are most at risk as their lungs are still developing and they are most likely to be outdoors when ozone levels are high.208 A cohort study followed 3,535 children in various communities in Southern California for five years, and 265 of the subjects were diagnosed with asthma.209 In children playing three or more sports in communities with high ozone levels, the relative risk of developing asthma was 3.3 times that of children playing no sports. Spending time outside in these areas was likewise positively associated with asthma (relative risk of 1.4), whereas playing sports in areas with low ozone levels was not (relative risk of 0.8).209

Solutions

1. Carbon Air Filtration

Carbon filters can remove 60% to 70% of ozone from the passing air, according to a test performed in Sacramento, California, by Lawrence Berkeley National Laboratory.210

4. Nitrogen Dioxide

Exposure to nitrogen dioxide (NO2) can lead to respiratory effects including airway inflammation and increased symptoms in people with asthma.211 NO2 is a product of combustion and is mainly found near burning sources such as wood smoke and traffic combustion. The air in many indoor spaces has half the amount of NO2 as outdoor air. However, indoor areas containing gas stoves, fireplaces and cigarette smoke often have a high concentration of NO2 and require monitoring and good ventilation in order to be safe. Nitrogen dioxide and nitrogen oxide (NO), often formed simultaneously during combustion processes, are collectively classified as NOX.211

NO2 can be detected by smell at 100 to 400 ppb, or 0.4 ppm. Exposure to 150 ppm (150,000 ppb) or more of NO2 can cause death from pulmonary edema,212 and exposure of 174 ppm for one hour has been associated with a 50% chance of mortality.213 Animals exposed to one ppm (1,000 ppb) of NO2 for several months show signs of chronic health issues.

EPA and ASHRAE’s annual limit for outdoor NO2 concentration is 53 ppb, with hourly peaks of less than 100 ppb 214. WHO’s annual guideline for NO2 is 40 µg/m³, with hourly peaks below 200 µg/m³ 101.

Health Effects

Respiratory System

Respiratory irritation. The EPA reports that the effects of NO2 are similar to allergens and can lead to cold-like symptoms and trigger asthmatic events when inhaled.214 NO2 also causes eye irritation and dryness of the nose and throat.214

Respiratory mortality. In the past, NO2 exposures have frequently occurred in crop storages in farm silos, where toxic levels of nitrogen are often produced after the silos are filled with an organic material.215 “Silo filler’s disease” is a well-known example of the morbidity and mortality associated with NO2 exposure, leading to symptoms such as respiratory tract irritation, bronchiolitis obliterans, pulmonary edema, and death.215

Upper respiratory symptoms. The EPA notes that breathing in air with high concentrations of NO2 can irritate the human respiratory system and aggravate respiratory diseases (such as asthma), leading to adverse respiratory symptoms, hospital admissions, and emergency room visits.216 A study analyzing the upper respiratory health of 1,854 schoolchildren (aged nine to 11 years old) found a significant association (odds ratio of 1.82) between upper respiratory illnesses, such as a running nose, a cough or hoarseness, and exposure to moderate levels of NOX (maximum concentrations ranging between 49–502 µg/m³).217

Respiratory and Immune Systems

Asthma. A three-year cohort study carried out in seven communities in Japan determined an average NO2 pollution for each community and assessed the respiratory symptoms of 842 schoolchildren via questionnaires.218 A 10 ppb increase in outdoor NO2 was associated with a 76% increase in the incidence of wheezing, and a 210% increase in the incidence of asthma (odds ratio of 1.76 and 2.10, respectively).218 Several studies have shown that children are likely affected by the use of gas stoves in the home and that emissions from them are likely triggers for asthma. While this link has been shown in children, it has not been verified to the same degree in adults.219

Cardiovascular System

Cardiopulmonary mortality. A 2006 study suggested an association between elevated NO2 exposure and a 57% higher risk of cardiopulmonary mortality, after adjusting for socioeconomic factors and smoking.220

Solutions

1. Vehicle Idling Limits

Cars use more fuel and cause more engine wear when they idle for more than 30 seconds compared with turning off and restarting the engine.112 Cars and trucks that use gas generate approximately 60,000 µg and heavy-duty diesel vehicles generate 560,000 µg of nitrous oxides per minute of idling.113 By limiting vehicle idling on nearby roads and driveways, buildings can reduce a local source of particulate matter pollution.

2. Operable Windows

Windows that can be opened and closed by the people in the building or automated systems can rapidly increase or decrease the amount of outside air entering a building, depending on the outdoor air conditions. This combined with filtration or air conditioning is effective at reducing ozone and NO2 levels.110

3. Kitchen Exhaust Hoods

Gas stovetops and ovens produce nitrogen dioxide. Venting hoods over the stove can greatly reduce this pollution.111

5. Radon

Radon is a naturally occurring gas that results from the radioactive breakdown of uranium (Figure 13). The primary health risk from radon exposure is lung cancer.221

Radon is odorless, colorless and tasteless, and enters working and living spaces through cracks in building foundations.222 The gas can accumulate in buildings, especially in confined areas such as attics and most commonly, basements. It leaves the surrounding soil and enters basements because of a slight pressure difference driven by buoyant natural circulation that results from temperature differences indoors. Water from deep wells drilled into rock may contain high radon levels, and homes that draw water from such sources may introduce radon through the plumbing.222

FIGURE 13: RELATIVE HALF-LIFE OF PRODUCTS FROM URANIUM DECAY.223
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Radon is a radionuclide that decays through short-lived progeny (radon daughters) before eventually reaching its stable end product, lead.224 Throughout the decay process, radon and its products emit ionizing particles that attach to particulate matter in the air. As radon decays into polonium, it releases atomic particles made up of two protons and two neutrons. These “alpha” particles are ionizing but are blocked by most matter, such as the thin layer of dead cells, which make up the outermost layer of skin. Nevertheless, if radon gas is inhaled, the alpha particles will directly impact the lung cells and potentially cause mutations.224

Radon’s radioactive by-products tend to attach to particulate matter such as elemental carbon. These particles are then carried and deposited in the lungs. Thus, in buildings with a higher concentration of indoor particulate matter or for those who smoke, radon poses a larger threat.225

The International Standard (SI) unit of measure for radioactivity is the Becquerel (Bq) and in the U.S., the more commonly used unit is the Curie (Ci).226 One Bq corresponds to the transformation (disintegration) of one atomic nucleus per second, which is equal to 2.7 x 10(^-11) Ci (0.27 pico curie, or pCi). Average indoor U.S. radon levels are estimated to be 1.3 pCi/L, and outdoor air carries about 0.4 pCi/L. The EPA suggests homeowners with radon levels above four pCi/L to take steps to reduce the levels in their homes, with some individual states in the U.S. requiring radon abatement in homes prior to sale 226. Radon in water typically adds one pCi/L to the indoor air levels for every 10,000 pCi/L in water.227

FIGURE 14: RADON AND PREVENTABLE DEATHS IN THE UNITED STATES.226
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Health Effects

Respiratory and Endocrine Systems

Lung cancer. Among nonsmokers, indoor exposure to radon is the leading cause of lung cancer and the second overall leading cause of lung cancer.229 Radon is responsible for about 21,000 deaths per year in the U.S.229

A 2006 study analyzed data from seven North American case-control studies using long-term α-track detectors to assess residential exposures to radon and to investigate a possible association with an elevated risk of lung cancer.230 An 11% increase in odds (odds ratio of 1.11) was estimated after exposure to radon at a concentration of 100 Bq/m³ (2702 pCi/L) in the exposure timeframe of five to 30 years. Reducing the data to a subset with higher precision regarding the radon exposure led to a further increase in risk. This was one of the first studies to provide direct evidence on the correlation between radon exposure and elevated risk of lung cancer outside of the occupational setting of mining, which has higher exposure dosages.230

Solutions

1. Adequate Ventilation

In its Consumer’s Guide to Radon Reduction, the EPA recommends increased ventilation of spaces to reduce radon levels.231 This can be achieved through passive ventilation (e.g., by installing additional vents) or by temporarily opening windows, as well as through active ventilation using fans to expedite air exchange. Heat recovery ventilators (HRVs), which are especially effective in removing radon from basements, use the expelled indoor air to heat or cool the introduced outdoor air, maintaining a comfortable indoor environment.231

2. Sealing of Radon Entry Routes

In addition to increasing ventilation, the EPA recommends sealing cracks in basements and foundations, through which radon may enter the home. This solution makes ventilation techniques more efficient and saves energy.231

Volatile Organic Compounds (VOCs)

Unlike ozone and nitrogen oxides, which mainly form in outdoor areas, some VOCs arise from newly installed products or activities within buildings. Materials used for ongoing maintenance, such as cleaning products, air fresheners, pest control chemicals, and furniture polish can increase VOC levels for a period of time, and their presence indoors is commonly two to five times higher than outdoor levels.10 Furthermore, human occupancy is responsible for the generation of VOCs from odors, personal care products, perfumes, shoe polish, hair spray, and electronic devices. However, not all VOCs or levels of exposure are anthropogenic or harmful.10

Semi-Volatile Organic Compounds, or SVOCs, are a subcategory of VOCs that have a boiling temperature above that of water (between 240°C and 400 °C).232 Nevertheless, SVOCs can vaporize from products, as they are not bound to the materials and can become distributed throughout the indoor environment. SVOCs are present at very low levels in some commercial products, such as plasticizers in flooring, pesticides, and flame-retardants in insulation, and many have known toxicological effects at levels of exposure significantly higher than those generally experienced in buildings.232

According to the EPA, the health effects of high levels of exposure to some VOCs can include eye, nose, and throat irritation, headaches, loss of coordination, nausea, and damage to the liver, kidney, and central nervous system.10

New furniture and newly installed building materials—including specifically composite wood products—can be the largest source of harmful indoor VOCs that decline with time and use.233 While individual sources may have low VOC emissions, the cumulative effects of multiple products and materials used inside a home or building can elevate concentrations. It is important to understand the total level of VOC exposure over time given that many products labeled “low VOC” can be found in combination with other products.233

Central nervous system effects (e.g., dizziness) may be an early indication of VOC exposure, as the brain is believed to be an easy target due to its high lipid content and steady supply of blood, especially given that VOCs are known to be able to permeate lipid membranes.15 Sick building syndrome (SBS) is used to describe acute health affects linked to building occupancy but without a specific diagnosis of a disease or a directly identified cause.15 SBS is most frequently attributed to poor ventilation and has also been associated with off-gassing by some newly installed building materials and furnishings.15 A study involving 12 California buildings found an association between VOC exposure metrics and SBS symptoms.234 One of the seven VOC-based metrics tested, the “irritancy/principal components” metric, was a statistically significant predictor of general symptoms (i.e., eye, nose, throat, and skin irritation). The irritant symptoms were found to be associated with carpet VOC emissions (styrene) and cleaning products (2-butoxyethanol and 2-propanol).234

In combination with indoor or outdoor NO2 and sunlight, VOCs react to produce ozone.101 They can also react with nitrogen oxides or O3 to produce new substances and secondary aerosols, which have been shown to cause sensory irritation symptoms.235 Few regulatory agencies have limits for VOC concentrations in the air and instead limit emissions from products.

For more information on Volatile Organic Compounds, refer to the Materials WELLography™.

1. Benzene

Benzene is a volatile organic hydrocarbon with the molecular formula C6H6.236 It is a natural component of crude oil and is found in gasoline and cigarette smoke. Benzene is colorless and highly flammable. It is used in the production of many common products, such as gasoline, plastic, rubber, and synthetic fabrics like nylon and polyester, however, in building materials used indoors it cannot be measured in the final product.236

Acute health effects associated with continued high levels of exposure to benzene over a significant period of time include neurological symptoms, as well as skin, eye, and lung irritation. Average lifetime cancer risk from exposure to 177 studied air pollutants (excluding radon) at typical outdoor levels is estimated to be between 1 in a million and 25 in a million. The biggest component of this risk, making up 25% of the total risk, is benzene, largely generated by vehicular traffic.237

Health Effects

Endocrine and Immune Systems

Leukemia. Benzene is classified as a Group 1 known human carcinogen by the IARC.238

An epidemiological case-control study of 79 individuals working in the Australian petroleum industry assessed the linkage between benzene exposure and the risk of leukemia.239 For a cumulative benzene exposure above eight ppm-years (parts per million–years), an increased risk of leukemia was found with an odds ratio of 11.3, and risk further increased with higher exposure.239

Another case-control study, with 765 cases of leukemia in children under the age of 15, found a significant association between acute childhood leukemia and residence near a gas station or auto repair garage (odds ratio of 1.9 and 1.6, respectively).240 The authors concluded that low-level benzene exposure has a role in the development of childhood leukemia.240

Nervous System

Headaches and fatigue. Chronic and acute exposure to levels above OSHA limits often leads to nervous impairment 241. A study with 121 workers investigated the neurological impact of chronic exposure (6 to 15.6 ppm for two to nine years) to benzene. Over 60% of the workers complained of headaches, fatigue, difficulty sleeping, and memory loss. It should be noted that the workers in the study were also chronically exposed to toluene, but at levels lower than 1.5 ppm (5 mg/m³). The EPA also notes that exposure to high concentrations (250 to 3,000 ppm) of benzene can cause dizziness, headache, and vertigo.241

Solutions

1. Pollutant Restriction and Abatement

The WHO recommends eliminating the use of benzene by promoting, “the use of alternative solvents in industrial processes, glues and paints,” as well as, “avoid[ing] domestic use of benzene-containing products”.242

2. Vehicle Idling Limits

Cars use more fuel and cause more engine wear when they idle for more than 30 seconds compared with turning off and restarting the engine 112. In 1999, cars and trucks were responsible for almost half of all benzene emissions in the U.S.237 By limiting vehicle idling on nearby roads and driveways, buildings can reduce the local sources of VOC pollution.

3. Carbon Air Filtration

Carbon filtration has shown to be an effective method of removing airborne benzene. One study showed a 90% reduction in benzene when a steady flow of waste gas passed through a carbon filter at a steady rate of flow.243 Standalone air purifiers using a combination of activated carbon, photocatalytic filters, and manganese dioxide are effective at removing benzene from indoor air.244

2. Formaldehyde

Formaldehyde is used as a precursor in the production of many complex compounds and is used in many industrial applications.245 At room temperature, it is a gas.245 Exposure to formaldehyde in indoor environments can occur through off-gassing from wood-based products assembled with urea-formaldehyde, but can also come from paints, varnishes, floor finishes, or cigarette smoke.246 EPA reports that Salthammer et al. (2010) reviewed from studies from 2005 or later and concluded that typical indoor air levels are 16-32 ppb.247

The WHO has established exposure guidelines for formaldehyde in non-occupational settings at 100 ppb for 30 minutes.248 These are levels at which the risk of upper respiratory tract cancer in humans can be considered negligible.248 The U.S. Department of Housing and Urban Development sets indoor ambient formaldehyde levels at 400 ppb for manufactured homes, adding restrictions for component standards, plywood material emissions at less than 200 ppb and particle boards at 300 ppb.249

FIGURE 15: FORMALDEHYDE EXPOSURE RANGES.250
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Health Effects

Nervous System

Sensory irritations. Formaldehyde generally causes eye irritation at 310 ppb. However, some sensitive individuals may experience symptoms at 100 ppb.251

Neurobehavioral performance. Neurological effects of formaldehyde exposure have been observed in humans breathing 0.1 to 0.5 ppm.252

Respiratory System

Childhood asthma. According to the Agency for Toxic Substances and Disease Registry, there is a possible relationship between formaldehyde exposure the development of childhood asthma or asthma-like symptoms.252 A systematic review of seven (mostly cross-sectional) studies included data on a possible association between formaldehyde exposure and asthma in children, suggesting a positive relationship between formaldehyde levels and childhood asthma (odds ratio of 1.17 per 10 µg/m³ increase.253

Respiratory diseases. A study of 298 children suggests a positive relationship between formaldehyde exposure and respiratory symptoms in children.254 The children completed questionnaires on chronic respiratory symptoms and had their peak expiratory flow rates measured up to four times per day, and formaldehyde levels in their homes were measured for two one-week periods. Peak expiratory flow rates were 10% lower with formaldehyde exposure levels as low as 30 ppb, with greater effects seen in children with asthma.254

Solutions

1. Operable Windows

Windows that can be opened by the people in the building or automated systems can rapidly increase the amount of outside air entering a building. While this is effective at reducing formaldehyde levels,255 care must be taken to avoid introducing ambient air, which may be higher in other pollutants, such as ozone and particulate matter.

The ATSDR measured formaldehyde levels in 96 temporary-housing trailers, very similar to those used for people displaced by Hurricane Katrina.256 They measured formaldehyde levels of 0.01 to 3.66 ppm, with an average of 1.04 ppm, in the closed and unventilated trailers. Opening the windows for two weeks led to significant reductions in formaldehyde levels, to 0.09 ppm (90 ppb) on average.256

2. Adequate Ventilation

The ATSDR measured lower formaldehyde levels in housing trailers with the air conditioning units running and found much higher levels in closed and unventilated trailers. Average levels of 0.39 ppm were measured in ventilated trailers compared to 1.04 ppm in closed and unventilated trailers.256

3. Material Constraints

The EPA suggests reducing the amount of indoor formaldehyde by buying composite-wood products that have been certified as compliant by the American National Standards Institute (ANSI) or the California Air Resources Board Airborne Toxic Control Measures (ATCMs) to Reduce Formaldehyde Emissions from Composite Wood Products.257

4. Carbon Air Filtration

Activated carbon filters are effective at adsorbing formaldehyde from the circulated air. The concentration of formaldehyde in air passing through these filters can be reduced by 20% with total removal efficiency up to 40%.258 In buildings without central air systems, standalone air purifiers using a combination of activated carbon, photocatalytic filters, and manganese dioxide have also been shown to be effective at removing formaldehyde from indoor air.255

5. Controlling Temperature

The ATSDR found a highly positive correlation between formaldehyde levels in temporary-housing trailers and indoor temperature (with windows closed): Formaldehyde levels when the trailer was at 80°F were twice as great compared with when it was at 70°F.256 The EPA suggests that high temperatures accelerate formaldehyde emissions from indoor sources,257 for example during building pre-occupancy period.

6. Controlling Humidity

Keeping humidity levels low can decrease indoor formaldehyde emissions. A study carried out chamber experiments with sample materials from trailers and found that an increase of relative humidity up to 35% led to increased formaldehyde emissions from the materials by a factor of 1.8–2.6.260 An additional study found a positive correlation between the emission rate of formaldehyde found in building materials and absolute humidity, with high humidity associated with greater emission rates.261

7. Kitchen Exhaust Hoods

Gas stovetops and ovens produce formaldehyde. Venting hoods over the stove can greatly reduce this pollution.111

Polycyclic Aromatic Hydrocarbons (PAHs)

Polycyclic aromatic hydrocarbons are atmospheric pollutants consisting of two or more fused hydrocarbon rings.262 PAHs are very widespread organic pollutants and originate from combustion processes in both indoor and outdoor sources such as vehicle exhaust, cigarette smoke, home heating, and laying tar. According to the WHO, “life-long exposure to PAHs at concentrations commonly observed in European or North American cities is associated with up to 50 excess cases of lung cancer per 1,000,000 people”.262

1. Benzo[a]pyrene (BaP)

Benzo[a]pyrene (BaP) is one of the most potent carcinogenic PAHs. The risk of PAH exposure is higher in houses with smokers or other forms of indoor combustion and improper ventilation.262 WHO does not consider any detectable levels of BaP to be safe.248 The EPA does not regulate BaP in air, but OSHA’s permissible eight-hour average is 200 µg/m³, and NIOSH’s recommended exposure limit is 100 µg/m³ average over a 10-hour period.263

Health Effects

Endocrine System

Multiple cancers. BaP is associated with chromosomal replication errors, leading to multiple types of cancer.264

Reproductive and Endocrine Systems

Fetal abnormalities and death. Fetal exposure to BaP is associated with developmental abnormalities, as well as with an increased incidence of tumors later in adulthood.264 Given the greater likelihood to play in and around soils contaminated with BaP, children are at higher risk of exposure than adults.264

Nervous System

Cognitive development. A 2012 study found a correlation between prenatal exposures to New York City’s environmental PAH levels and symptoms of anxiety/depression and attention problems in 253 children, ages six and seven.265 PAH exposures of nonsmoking women during pregnancy as well as BaP-specific biomarkers in subjects’ maternal and cord blood were measured, and their children’s development was assessed using the Child Behavior Checklist (CBCL). The study found an association between increased prenatal exposure to PAHs and anxiety/depression as well as attention problems on the CBCL. It further concluded that maternal exposure could impact the children’s cognitive development and ability to learn.265 Additionally, a 2015 prospective cohort study of 40 children found an association between prenatal PAH exposure and changes in cognition and behavior in childhood. Specific effects included slower processing speed, symptoms of ADHD, and externalizing problems (which include maladaptive behaviors that individuals direct towards their environment).266

Solutions

1. Kitchen Exhaust Hoods

Frying, broiling, and sautéing are major sources of indoor PAH. Venting hoods over the stove can significantly reduce this pollution.111 264

Smoking

In 2013, an estimated 42.1 million people (or 17.8% of adults) were cigarette smokers in the U.S.267 Worldwide, there are more than one billion tobacco smokers, nearly 80% of whom come from low- or middle-income countries.268 Based on the EPA’s 24-hour air quality data from 2007 to 2009, it is estimated that the inhalation of ambient PM2.5 in Los Angeles (~343 µg a week) is equivalent to smoking four cigarettes.126

1. Tobacco Smoke

Cigarettes are the most common tobacco consumption method, but other tobacco products are gaining popularity. In India, a type of cigarette called a bidi, which is tobacco wrapped in a leaf, is more popular than a regular cigarette. In Indonesia, the kretek is a common type of tobacco cigarette that is blended with cloves. Shisha, a blend of fruits, oils, and dried plants smoked in a water pipe known as a hookah and originating from the Middle East is growing in popularity around the world.

The majority of tobacco products contain the compound nicotine, which is rapidly delivered to the brain when inhaled. Because nicotine is habit-forming, long-term smoking makes quitting difficult due to the withdrawal symptoms associated with cessation. In addition to nicotine, cigarettes contain about 600 ingredients that form over 7,000 compounds when burned, at least 69 of which are known to be carcinogenic.269 However, the consequences related to tobacco smoke usually do not manifest until many years after beginning smoking.270

The number of smokers worldwide is expected to continue increasing.271 WHO estimates that six million people a year die from smoking.268 Smoking-related deaths could reach eight million per year by 2030 if the growth rate for smoking tobacco products does not slow.272

According to the WHO, 18% of the world’s population today is protected by smoke-free laws. Smoke-free legislation has been implemented in large parts of the U.S., Canada, Europe, South Africa, Australia, Brazil, India, and other countries.273 These policies are enforced in schools, private and public workplaces, and public spaces, and are vital in helping prevent the dangers of secondhand smoke of which there is no safe exposure level.274 In addition to smoking, secondhand smoke is a serious and preventable cause of morbidity and mortality, and since 1964 has been the cause of over 2.5 million deaths among nonsmoking individuals in the U.S. alone.274

Health Effects

Respiratory System

Chronic obstructive pulmonary disease (COPD). As an active (mainstream) and passive (second hand) inhalant, tobacco smoke has direct adverse effects on the respiratory system COPD.275 COPD, which includes emphysema, was the first respiratory-related illness linked to smoking in the Surgeon General’s 1964 report. Annually, approximately 127,600 deaths in the U.S. are attributed to smoking-induced COPD.275

Tuberculosis (TB). While tuberculosis is no longer a prevalent disease in the U.S., it is still a prominent threat in the developing world. A nested case-control study in India compared the smoking practices of 85 men with tuberculosis to 459 randomly selected age- and gender-matched controls and found a positive association (odds ratio of 2.48) between tobacco smoking and tuberculosis.276 The association had a strong dose-response relationship, indicating that smokers are more likely to catch tuberculosis than nonsmokers.276 A prospective cohort study of 17,699 Taiwanese individuals found that smoking tobacco was associated with a twofold increased risk of active tuberculosis. Additionally, researchers identified a significant dose-response relationship for cigarettes smoked per-day, years of smoking, and pack-years with the risk of active tuberculosis.277

Respiratory and Immune Systems

Asthma. A large prospective cohort study in Germany of almost 3,000 individuals observed an association between smoking and incidences of wheezing or diagnosed asthma.278 Subjects, aged 9 to 11 years at the beginning of the study, underwent medical assessment and received follow-up questionnaires assessing their health and living conditions approximately seven years later. Compared with nonsmokers, smokers had an increased risk ratio of 2.76 for wheezing (without a cold) and a 2.56 increased risk ratio for diagnosed asthma.278

Respiratory and Endocrine Systems

Lung cancer. Smoking tobacco products can lead to the development of lung cancer, the most common cancer associated with smoking. Lung cancer is estimated to have been responsible for 137,989 deaths in the U.S. between 2005 and 2009, or approximately 29% of all smoking-attributable deaths.275 The risk of lung cancer associated with smoking has increased over time, presumably due to changes in the ingredient composition of cigarettes.279

Digestive and Endocrine Systems

Colorectal cancer. Cancer of the colon or rectum, sections of the lower intestinal tract, has been added to the health effects causally linked to smoking in the 2014 Surgeon General’s Report.280 A review of 27 studies found a positive association between smoking and an increased risk of colorectal cancer. Furthermore, it is estimated that one out of five cases of colorectal cancer in the U.S. may be attributable to tobacco use.281

Liver cancer. Many studies have confirmed a causal link between smoking and an elevated risk of liver cancer. A 2009 meta-analysis of studies examining the link between smoking and liver cancer confirmed that smoking increases the risk of liver cancer.282 Additionally, the U.S. Department of Health and Human Services and the IARC both note a positive relationship between smoking and liver cancer.280 282

Endocrine System

Type 2 diabetes. A systematic review and meta-analysis of 25 prospective cohort studies with 1.2 million participants and almost 46,000 incidences of diabetes over 5 to 30 years found a positive association between smoking status and type 2 diabetes.283 The pooled adjusted relative risk of developing type 2 diabetes for a smoker was 1.44 times that of a nonsmoker. Additionally, a dose-response relationship was observed, with lighter smokers experiencing lower risks compared to heavy smokers.283

Cardiovascular System

Cardiovascular disease. Cardiovascular disease is responsible for a significant portion of smoking-attributable deaths in individuals 35 years of age or older in the U.S.280 Exposure to tobacco smoke is associated with accelerated atherosclerosis and increased risk of acute myocardial infarction, stroke, aortic aneurysm, peripheral arterial disease, and sudden death. The risk of cardiovascular disease rises sharply with the use of tobacco or consistent exposure to secondhand smoke.280

Reproductive System

Erectile dysfunction. The 2014 Surgeon General’s Report indicates that there is sufficient evidence to demonstrate a causal relationship between smoking and male sexual dysfunction.280 Studies indicate a plausible mechanism by which tobacco may be responsible for altering the blood flow that is required for an erection to occur, similar to the effects of heart disease on coronary circulation.280

Birth defects. A systematic review of published scientific literature from 1959 to 2010 identified 172 articles that reported an association between non-chromosomal birth defects and smoking during pregnancy.284 The data, which included almost 175,000 cases and more than 11.6 million controls, found that smoking during pregnancy was associated with increased risk of limb reduction defects (odds ratio of 1.26), clubfoot and orofacial clefts (odds ratio of 1.28), defects of the eyes (odds ratio of 1.25), and gastrointestinal system (odds ratio of 1.27).284

Immune System

Rheumatoid arthritis. It is likely that environmental factors contribute to the development of rheumatoid arthritis (RA), a severe inflammatory arthritis. A prospective analysis of over 100,000 women (of whom 680 were diagnosed with RA) explored the risk of developing RA among current or former smokers and those who had never smoked.285 Compared to those who had never smoked, the relative risk of developing RA among current and former smokers was 1.43 and 1.47, respectively.285

Nervous System

Age-related macular degeneration (AMD). According to the 2014 Surgeon General’s Report, there is sufficient evidence to infer a causal link between smoking and an increased risk of AMD.280 While the risk of AMD is greatest for current smokers, there is also a significantly greater risk for former smokers compared to individuals who have never smoked.280

Solutions

1. Smoking Ban

To protect people from secondhand smoke, smoking should be prohibited in all (indoor and outdoor) public spaces. Smoke-free laws are already enforced in many schools, private and public workplaces, and public spaces around the world.273

A systematic review of smoke-free policies by the CDC’s Task Force on Community Preventive Services found strong evidence that these types of policies not only reduce the prevalence of tobacco use, exposure to secondhand smoke, initiation of tobacco use among youth, and tobacco-related morbidity and mortality, but they also increase the number of individuals who quit using tobacco products.286 Similar results were found in the Surgeon General’s 2014 report, The Health Consequences of Smoking—50 Years of Progress,280 as well as a report by the Campaign for Tobacco-Free Kids.287

Research evaluating the effects of smoke-free legislation suggests that these policies have positive effects on respiratory health288 and lower the risk of smoking-related cardiac and cerebrovascular diseases.289 A systematic review of smoke-free workplaces concluded that these policies reduce total cigarette consumption per employee by 29%.290 In one study, researchers tracked the number of respiratory and cardiovascular hospital admissions attributable to smoking after the implementation of smoking bans. These numbers were compared to admissions in counties without smoking bans, as well as admission rates prior to the smoke-free legislation. The study found that after the implementation of smoking bans, hospital admission rates for cardiovascular and respiratory-related diseases decreased by 39% and 33%, respectively.291

A major benefit of no-smoking policies is protecting people from the harms of secondhand smoke. Additionally, smoking bans have been shown to have significant effects on reducing levels of various chemicals associated with tobacco smoke in indoor environments. An exposure study linked the introduction of a smoking ban in Ireland to a reduction of benzene levels in 26 Dublin pubs by 80.2%, and a reduction of PM2.5 levels in 42 pubs by 83%.292 Additionally, a study conducted in Rome, Italy noted a decline in UFPs in hospitality venues after the implementation of an indoor smoking ban.293 Mean amounts of UFPs in the 47 establishments dropped from 76,956 pt/cm³ (particles per cm³) before legislation to 51,692 pt/cm³ 12 months post-legislation.293 Another study measured particle-bound PAHs (PPAHs), including BaP, in seven Boston pubs before and after the implementation of a smoking ban (ventilation rates in the pubs were within ASHRAE design parameters). In six of the seven pubs, PPAH levels were 10 times higher before the smoking ban (61.7 ng/m³) than afterward (6.32 ng/m³).294 Finally, a study in Saõ Paolo, Brazil measured CO levels in 585 hospitality venues before and 12 weeks after the implementation of smoke-free legislation. After implementing the smoking ban, the mean indoor CO levels had dropped from 4.57 ppm to 1.35 ppm, and in open areas, they had decreased from 3.31 ppm to 1.31 ppm.295

2. Smoking Cessation Programs

Smoking cessation programs, which include counseling and the use of FDA-approved medications, have been shown to reduce smoking rates successfully.296 297 In addition to behavior change, there may be economic benefits associated with reduced smoking rates. One study concluded that on average, U.S. employers pay an additional $5,816 for each smoker on their payroll.298 Furthermore, some research estimates that smoking contributes to over $150 billion in productivity losses in the U.S. each year.298

Explanations of Solutions

Particle Filters

Ventilation expels indoor air and replaces it with outdoor air.74 If the replacement air contains ozone, diesel particulate matter, or other pollutants, the air ducts will simply deliver dirty air back into the building. In order to prevent this from happening, ventilation systems require filtration. Different filters address different contaminants and are best used in combination (Figure 16).74

FIGURE 16: A MULTISTAGE APPROACH TO CLEANING AIR.74
expand this figure

Media Filteration. ASHRAE, in its Standard 52.2, assigns filters a Minimum Efficiency Reporting Value (MERV).43 The MERV number describes the number of different types of particles a filter removes when operating at the least effective point in its life. Although somewhat counterintuitive, filters become increasingly effective over time, as particles lodge in the mesh, reducing the open areas through which some may be able to pass in a newer, cleaner filter. This increased particle loading has increasing energy requirements, as more effort is required to push air through the filter.

Figure 17 summarizes the effects that different MERV filter levels have on air quality. In each category, the filter removes at least 85% of all contaminants larger than the range listed and a smaller fraction of those particles within the range.74 Within each level grouping, filters with higher designations (8, 12, etc.) remove more of the contaminants of the listed size.43 74

FIGURE 17: CLASSIFICATION OF MERV RATINGS74
expand this figure

MERV 1 to 4 do not address most of the particles harmful to people and are mainly used to protect mechanical and electronic devices. ASHRAE standards require any building with a central HVAC system to use MERV filters of level 8 or higher.74

Filters with MERV levels between 17 and 20 and are used in cleanrooms and pharmaceutical manufacturing facilities.74 Due to their typical use in scientific rather than commercial, residential, and institutional buildings, High Efficiency Particulate Air (HEPA) filters are governed by the Institute of Environmental Sciences and Technology rather than ASHRAE.74 HEPA’s extreme filtration results in a large pressure drop, which limits the quantity of air the device, can filter. As a result, these filters are often installed in bypass configuration, which provides high-quality filtration to a portion of the air, while leaving the remainder untreated. This process can result in unfiltered outside air circumventing the HEPA filter and entering the building.74

Freestanding air purifiers can remove impurities from a limited quantity of air through a variety of treatment and filter technologies. They provide flexibility of application where there are no ducts and air handlers, but can typically only clean the air in a single room.

Electrostatic Filters. By imparting a charge to airborne particles, electrostatic filters can then attract particulate matter and remove the particles from the air.299 The gaps in the mesh are larger than in media filters, which allow more airflow for a given design of fans, while the electric adhesion maintains filtration capacity. However, the use of low-efficiency filters upstream can remove the large particles before they reach the mesh and therefore help control ozone generation. When used and maintained properly, ozone molecules produced by electrostatic systems usually decay before reaching unhealthy concentrations.299

Carbon Air Filtration. Carbon air filters work by adsorbing many organic and reactive airborne contaminants.300 Carbon filters remove most gaseous contaminants, except CO, and must be preceded by traditional filters to remove particulates that would otherwise clog their pores. Typical carbon filters can be installed directly into ducts and last 6 to 12 months if used with dust-free air. They are also often included in freestanding air purifiers.

Ultraviolet Germicidal Irradiation (UVGI)

UVGI is a disinfection technique that can effectively destroy microorganisms (or prevent them from replicating) by using short wavelength UV waves, thus causing DNA damage.301 UVGI systems usually use low-pressure mercury discharge lamps that emit 254-nanometer wavelength UV rays. In addition, the lamps produce some visible light that humans see as blue light.301 UVGI systems are often used in crowded environments and are installed in the ductwork of ventilation systems as well as in the open spaces in the upper parts of the room. To prevent human exposure to UV rays, the source of the rays has to be shielded.301 Additionally, the area in which UV irradiation takes place should be adequately ventilated, as ozone can be generated by UV light.

UV treatment aids in stopping the spread of microscopic life rather than purifying the air, as it does not remove dead biological contaminants that can still trigger allergies.

Photocatalytic Oxidation (PCO)

Photocatalytic oxidation is a reaction between a surface coating, such as titanium dioxide (TiO2), and oxygen to turn VOCs into CO2 and to kill and decompose bioaerosols.302 PCO can be active or passive. Active PCO systems use a high-surface area support that is irradiated with ultraviolet light in order to trap VOCs in HVAC systems. Under UV irradiation, the compound then reacts with a coating applied to the support and converts the undesirable contaminant to CO2 and water (or other end products).302 Passive PCO systems, which are still in the experimental stages of development, are similar to active ones. Instead of being incorporated into HVAC systems and using UV light, they are incorporated into building surfaces (e.g., painted walls) and use ambient light to activate the catalysts.302

Dehumidification

Dehumidifiers are devices used for removing moisture from the air in order to reduce the potential for growth of molds or dust mites.49 Dehumidifiers are especially useful in environments that tend to collect humidity, such as garages and basements.49 Dehumidifiers work by taking in air and running it through cold coils, thus causing any moisture from the air to condense. The air is then passed on to warm coils and out into the room. The water that condenses on the coils is collected and empties into a drain or has to be emptied manually.49

The EPA recommends that to prevent the establishment and growth of indoor pests, relative humidity indoors should be kept between 30% and 50%.92 Humidity toward the bottom of the range is better in terms of air quality, but extremely low moisture levels may lead to dry or itchy skin, eyes, or throat.303

Smoking Ban

Smoking bans are laws and policies that prohibit the use of tobacco in public buildings and spaces, workplaces, schools, campuses, restaurants, hotels, hospitals, and other indoor and outdoor venues. Cities can regulate smoking through tobacco-specific legislations or regulations. Alternatively, they can look to the existing labor, occupational health and safety, human rights, and environmental statutes, as well as other regulatory instruments, to implement or enforce smoke-free rules.

Effective protection from exposure to tobacco smoke requires total smoke elimination.274 This means that only 100% smoke-free environments are adequate at protecting people from the harms of exposure to secondhand smoke. Separated indoor smoking areas, even if separately ventilated, are not an effective solution.274

Smoking Cessation Programs

Smoking cessation programs are meant to help smoking individuals quit smoking through the use of counseling and/or FDA-approved medications. They have been shown to reduce smoking rates, the number of cigarettes smoked, and exposure to secondhand smoke, and should be included as a workplace wellness program or benefit covered by employer-provided health insurance.297

Cessation programs can include group or individual classes, counseling sessions, and telephone quit lines that educate and support smokers who would like to quit.296 In addition, educational materials can be made available either in hard copy or as online resources. Cessation programs may also include FDA-approved medications as another tool to aid smokers in quitting.304

Walk-off Entry System

Walk-off entry systems employ specific surfaces to capture the dirt and pollutants that can be tracked indoors by shoes or clothes.305

When choosing a walk-off system, the individual needs of the space should carefully be evaluated. Weather conditions, number and frequency of visitors, and entryway size must be considered, as the choice of system can have implications for overall cleaning and maintenance costs. Depending on these variables, mats can have more scraping or wiping properties and varying moisture absorbing qualities. Entryway walk-off systems can also consist of metal grating to remove heavy dirt. An additional benefit is that mats can play an important role in providing safety on slippery surfaces.

The matting manufacturing company Notrax estimates that in public buildings with high pedestrian traffic, 1,000 people can deposit up to 24 pounds of dirt on entryway matting over a 20-day period. Matting can assist in removing up to 80% of dirt.305

Efficient and Healthy Cleaning Routine

To maintain a people-friendly and healthy environment, a regular cleaning routine, including vacuuming, sanitizing, and disinfecting of floors and surfaces, is essential.

In a double-blind intervention study from 2004 with 114 nonsmoking participants who had recently been complaining of mucosal irritations, it was shown that the intervention group, whose office spaces were comprehensively cleaned, compared with the control group whose spaces underwent a placebo treatment, experienced a reduction in irritation symptoms, as well as in nasal congestion.306

A long-term study monitoring the indoor environment of a nonproblem, multi-floor building suggests that an improved cleaning program has positive effects on indoor air quality by reducing airborne dust mass, total VOCs, and levels of culturable bacteria and fungi.307

Material Constraints

Building materials, furniture, fabrics, office equipment, and finishes should be chosen carefully after analyzing the material composition and known associated health impacts. Bans of certain toxic materials such as asbestos and lead are relatively obvious constraints, but many indoor objects perceived as safe may also emit pollutants such as VOCs, thus contributing to a hazardous background level of indoor air pollution.10 Composite materials that are well known to off-gas formaldehyde and low-level pollution can gradually add up to potentially adverse exposure levels.

Furthermore, VOCs can leak out of closed cans and sprayers filled with household cleaners, making it necessary to keep these products in areas that do not interact with house air.10

Protection and Care During and Following Construction

Construction processes often produce large amounts of dust and other pollutants. As such, areas undergoing renovation or construction should be given special consideration in order to minimize the creation of additional indoor pollution construction.308

High dust contamination can be a strain for any existing HVAC system and lead to the exhaustion of installed filters. Moreover, certain materials can adsorb VOCs and other particles set free during construction.308 Therefore, it is advisable to physically protect some areas from pollution exposure in order to minimize the spread and adsorption of pollutants throughout the building and onto furnishings and materials. Keeping this in mind, intelligent use of existing mechanical systems, careful construction sequencing, and a thorough cleanup after finalization of building procedures are recommended measures when renovating an indoor environment.

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