Epidemiology studies the causes, distribution, and control of disease in a population. It represents the application of quantitative methods to evaluate health-related events and effects. Epidemiology is traditionally subdivided into observational and analytical components; the focus may be descriptive, or may attempt to identify causal relationships. Some classical criteria for determining causal relationships in epidemiology are consistency, temporality, plausibility, specificity, strength of association, and dose/response (Hill 1965).

Observational epidemiology studies are generally performed with a defined group of interest because of a specific exposure or risk factor. A control group is selected on the basis of similar criteria, but without the exposure or risk factor present. A prospective study (cohort study) consists of observations of a specific group over a long time.

Examples of epidemiological investigations are cross-sectional, experimental, and case-control studies. Observations conducted at one point in time are considered cross-sectional studies. In experimental studies, individuals are selectively exposed to a specific agent or condition. These studies are performed with the consent of the participants unless the condition is part of the usual working condition and it is known to be harmless. Control groups must be observed in parallel. Case-control studies are conducted by identifying individuals with the condition of interest and comparing factors of interest in individuals without that condition.

Industrial or occupational hygiene is about anticipating, recognizing, evaluating, controlling, and preventing conditions that may lead to illness or injury, or affect the well-being of workers, consumers, and/or communities. Important aspects include identifying hazardous exposures and physical stressors, determining methods for collecting and analyzing contaminant samples, evaluating measurement results, and developing suitable control measures. Occupational hygienists work closely with toxicologists for understanding chemical hazards, physicists for physical hazards (e.g., ionizing radiation), and physicians and microbiologists for biological hazards.

Buildings are more than inanimate physical entities, masses of inert material that remain relatively stable over time. The building and its occupants, contents, and surroundings constitute a dynamic tetrad in which all elements affect each other. In fact, a building is a dynamic combination of physical, chemical, and biological dimensions. Buildings can be described and understood as complex systems. Some new approaches, based on the frameworks, tools, and methods used by ecologists to understand ecosystems, can help engineers understand the processes and microbes continually occurring indoors and how they affect the building’s inhabitants, durability, and function (Bassler 2009; Humphries 2012).

Building scientists need to understand the complex and bidirectional relationship between the physical/chemical parameters of a building and the microbiology of that environment. Attempting to control a single parameter (e.g., temperature) to regulate the growth of a single microbe (e.g., mold), for example, does not address the complexity of the system.

Microbiologists must recognize the importance of understanding all of the environmental variables that are present in a given habitat. Simply collecting microbes from surfaces or materials in a structure is not enough to understand the organisms’ behavior and relationships in the context of the building. Collecting appropriate information about the building (metadata) such as air turnover rates and material composition is essential to understanding the microbial communities that live inside it. Microbiologists must also be ever mindful of the need to distinguish between the occurrence of a microbe and the activity (metabolome) of a microbe or microbial community.

Culture-independent (genetic) methods of identifying microorganisms in microbiology are rapidly changing our understanding of the occurrence and nature of microbes in indoor environments [see Microbiology of the Built Environment network (www.microbe.net)]. These methods have increased tenfold the number of known bacteria over the past decade. Efforts to better understand the relationship between the indoor environment and its microbial ecology are yielding new knowledge about the complexity of the indoor environment as an ecosystem (Corsi et al. 2012).

Viruses require living cells for replication, so abiotic building components, strictly speaking, do not serve as a source of viruses. Viruses in buildings come from the building’s occupants. Building components or systems can provide surfaces that facilitate transmission (e.g., doorknobs), and some viruses can become airborne. A substantial body of literature compares airborne and other routes of transmission; from a building design and operations standpoint, though, avoid generalizations because transmission routes are not the same for all viruses.

Empirical data (Lowen et al. 2007) demonstrate that some airborne viruses (e.g., influenza) are inactivated more quickly at high humidity, and that low humidity rapidly reduces the size of respiratory droplets, thereby prolonging time aloft. Maintaining humidity in the range deemed comfortable to a majority of occupants reduces these effects that favor influenza transmission.

Much of the literature on fungi focuses on temperature and moisture, with some emphasis on moisture and nutrient availability, although there is sufficient nutrient content on most indoor surfaces: fungi can grow even on what appears to be clean glass. There is less literature on the factors determining bacterial species and survival indoors, in spite of the growing interest in the hygiene hypothesis and humans’ intimate relationships with both beneficial and harmful bacteria (e.g., probiotics). See Flanigan et al. (2001) for details.

Moisture on many surfaces supports the life, reproduction, and evolution of microorganisms. The microorganisms themselves produce chemicals, some of which can alter the pH of the surface and subsequent surface chemistry. Many additional microbes arrive on human skin, which sheds on a regular basis. Skin cells and the oils and other chemicals in and on them, as well the bacteria living on them, end up on the floor, furniture, and even the walls and windows.

When bacteria colonize stable surfaces, they often form complex communities. The structure and composition of these communities depend not only on the organisms present, but also on the conditions surrounding them: the moisture, chemicals, and other particles present on the surface or in the air nearby. Some of these communities may even develop into biofilms, which are very stable communities that are resistant to many antimicrobial compounds and can shelter pathogenic microbes. Bacterial communities sense the presence of other bacteria, and when they are enough of them to collectively affect their host, they all excrete chemicals that collectively affect the host and, in the case of human hosts, can make the bacteria more infectious (Bassler 2009).

Toxicology studies the influence of chemicals, particles, ultrafine particles, and bioaerosols on health. All chemical substances may function as toxins, but low concentrations prevent many, but not all, of them from being harmful. Defining which component of the structure of a chemical predicts the harmful effect is of fundamental importance in toxicology. A second issue is defining the dose/response relationships of a chemical and the exposed population. Dose may refer to delivered dose (exposure presented to the target tissue) or absorbed dose (the dose actually absorbed by the body and available for metabolism). For many substances, the time of exposure may be most important: low-level exposure during a specific week during pregnancy, for instance, may be critical, whereas higher doses later may have less of an effect.

Because permission to conduct exposure of human subjects in experimental conditions is difficult to obtain, most toxicological literature is based on animal studies. Isolated animal systems (e.g., homogenized rat livers, purified enzyme systems, other isolated living tissues) are used to study the effects of chemicals, but extrapolation between dose level effects from animals to humans is problematic.

Strategies for controlling exposures in the indoor environment include substitution (removal of the hazardous substance), isolation, disinfection, dilution ventilation, and air cleaning. Not all measures may be applicable to all types of hazards, but all hazards can be controlled by using one of them. Personal protective equipment and engineering, work practice, and administrative controls are used to apply these methods. Source removal or substitution, customarily the most effective measure, is not always feasible. Engineering controls (e.g., ventilation, air cleaning) may be effective for a range of hazards. Local exhaust ventilation is more effective for controlling point-source contaminants than is general dilution ventilation.

Hazard Analysis and Control Processes. The goal of hazard analysis and control processes is to prevent harm to people from hazards associated with buildings. Quantitative hazard analysis and control processes are practical and cost-effective. Preventing disease from hazards requires facility managers and owners to answer three simple, site-specific questions:

Seven principles comprise effective hazard analysis and control:

Exposures and Exposure Sources. In industrial environments, airborne particles are generated by work-related activities (e.g., adding batch ingredients for a manufacturing process, applying asphalt in a roofing operation, drilling an ore deposit in preparation for blasting). The engineer must recognize sources of particle generation to appropriately address exposure concerns. Dusts are generated by handling, crushing, or grinding, and may become airborne during generation or handling. Any industrial process that produces dust fine enough (about 10 μm) to remain in the air long enough to be inhaled or ingested should be regarded as potentially hazardous. In determining worker exposure, the nature of particles released by the activity, local air movement caused by makeup air and exhaust, and worker procedures should be assessed for a complete evaluation (Burton 2000).

Health Effects of Industrial Exposures. Pneumoconiosis is a fibrous hardening of the lungs caused by irritation from inhaling dust in industrial settings. The most commonly known pneumoconioses are asbestosis, silicosis, and coal worker’s pneumoconiosis.

Asbestosis results from inhalation of asbestos fibers found in the work environment. The U.S. Department of Health and Human Services (ATSDR 2001) characterizes the toxicological and adverse health effects of asbestos and indicates that asbestos-induced respiratory disease can generally take 10 to 20 years to develop, although there is evidence that early cases of asbestosis can develop in five to six years when fiber concentrations are very high. Asbestos fibers cause fibrosis (scarring) of lung tissue, which clinically manifests itself as dyspnea (shortness of breath) and a nonproductive, irritating cough. Asbestos fiber is both dimensionally respirable and durable in the respiratory system.

Silicosis, probably the most common of all industrial occupational lung diseases, is caused by inhalation of silica dust. Workers with silicosis usually are asymptomatic, even in the early stages of massive fibrosis (Leathart 1972). It is not considered a problem in nonindustrial indoor environments.

Coal worker’s pneumoconiosis (CWP, also known as “black lung”) results from inhalation of dust generated in coal-mining operations. The dust is composed of a combination of carbon and varying percentages of silica (usually <10%) (Alpaugh and Hogan 1988). Because of the confined underground work environment, exposures can be very high at times, thus creating very high doses. Data show that workers may develop CWP at exposures below the current dust standard of 1 mg/m³.

Exposure Standards and Criteria. In the United States, the Occupational Safety and Health Administration (OSHA) has established permissible exposure limits (PELs) for many airborne particles. PELs are published in the Code of Federal Regulations (29CFR1910.1000, 29CFR1926.1101) under the authority of the Department of Labor. Table 2 lists PELs for several common workplace particles.

Exposure Control Strategies. Particulate or dust control strategies include source elimination or enclosure, local exhaust, general dilution ventilation, wetting, filtration, and use of personal protective devices such as respirators.

The most effective way to control exposures to particles is to totally eliminate them from the work environment. The best dust control method is total enclosure of the dust-producing process, with negative pressure maintained inside the entire enclosure by exhaust ventilation (Alpaugh and Hogan 1988).

Local exhaust ventilation as an exposure control strategy is most frequently used where particles are generated either in large volumes or with high velocities (e.g., lathe and grinding operations). High-velocity air movement captures the particles and removes them from the work environment.

General dilution ventilation in the work environment reduces particulate exposure. This type of ventilation is used when particulate sources are numerous and widely distributed over a large area. This strategy is often the least effective means of control, and may be very costly if conditioned (warm or cold) air is exhausted and unconditioned air is introduced without benefit of air-side energy recovery. Ventilation and local exhaust for industrial environments are discussed more thoroughly in Chapters 31 and 32 of the 2019 ASHRAE Handbook—HVAC Applications.

Filtration can be an effective control strategy and may be less expensive than general ventilation, although increased pressure drop across a filter can add to variable fan power requirements, and maintenance adds to system operating cost.

Using personal protective equipment (e.g., a respirator) is appropriate as a primary control during intermittent maintenance or cleaning activities when other controls are not feasible. Respirators can also supplement good engineering and work practice controls to increase employee protection and comfort (Alpaugh and Hogan 1988). Consultation with an industrial hygienist or other qualified health professional is needed to ensure proper selection, fit, and use of respirators.

Exposures and Exposure Sources. Fibers are defined as slender, elongated structures with substantially parallel sides (as distinguished from a dust, which is more spherical). Synthetic vitreous fibers (SVFs) are inorganic fibrous materials such as glass wool, mineral wool (also known as rock and slag wool), textile glass fibers, and refractory ceramic fibers. These fibers are used primarily in thermal and acoustical insulation products, but are also used for filtration, fireproofing, and other applications. Human exposure to SVFs occurs mostly during manufacture, fabrication and installation, and demolition of those products, because the installed products do not result in airborne fiber levels that could produce significant consumer exposure. Simultaneous exposure to other dusts (e.g., asbestos during manufacture, demolition products and bioaerosols during demolition) is also important.

Health Effects of Exposure. Possible effects of SVFs on health include the following.

Cancer. In October 2001, an international review by the International Agency for Research on Cancer (IARC) reevaluated the 1988 IARC assessment of SVFs and insulation glass wool and rock wool. This resulted in a downgrading of the classification of these fibers from Group 2B (possible carcinogen) to Group 3 (not classifiable as to the carcinogenicity in humans). IARC noted specifically that “Epidemiologic studies published during the 15 years since the previous IARC Monograph’s review of these fibers in 1988 provide no evidence of increased risks of lung cancer or mesothelioma (cancer of the lining of the body cavities) from occupational exposures during manufacture of these materials, and inadequate evidence of any overall cancer risk.” IARC retained the Group 2B classification for special-purpose glass fibers and refractory ceramic fibers, but its review indicated that many of the previous studies need to be updated and reevaluated, because they did not include the National Toxicology Program’s Report on Carcinogens and the State of California’s listing of substances known to cause cancer.

Dermatitis. SVFs may cause an irritant contact dermatitis with dermal contact and embedding in the skin, or local inflammation of the conjunctiva when fibers contact the eye. Resin binders sometimes used to tie fibers together have, on rare occasions, been associated with allergic contact dermatitis.

Exposure Standards and Criteria. OSHA has not adopted specific occupational exposure standards for SVFs. A voluntary workplace health and safety program has been established with fibrous glass and rock and slag wool insulation industries under OSHA oversight. This Health and Safety Partnership Program established an 8 h, time-weighted average permissible exposure limit of 1 fiber per cubic centimetre for respirable SVFs.

Exposure Control Strategies. As with other particles, SVF exposure control strategies include engineering controls, work practices, and use of personal protective devices. Appropriate intervention strategies focus on source control.

Exposures and Sources. Combustion products include water vapor, carbon dioxide, heat, oxides of carbon and nitrogen, and combustion nuclei. Combustion nuclei, defined in this chapter as particulate products of combustion, can be hazardous in many situations. They may contain potential carcinogens such as polycyclic aromatic hydrocarbons (PAHs).

Polycyclic aromatic compounds (PACs) are the nitrogen-, sulfur-, and oxygen-heterocyclic analogs of PAHs and other related PAH derivatives. Depending on their relative molecular mass and vapor pressure, PACs are distributed between vapor and particle phases. In general, combustion particles are smaller (0.01 to 4 μm) than mechanically generated dusts.

Typical sources of combustion nuclei are tobacco smoke, fossil-fuel-based heating devices (e.g., unvented space heaters and gas ranges), and flue gas from improperly vented gas- or oil-fired furnaces and wood-burning fireplaces or stoves. Infiltration of outdoor combustion contaminants can also be a significant source of these contaminants in indoor air. Therefore, combustion nuclei are important in both industrial and nonindustrial settings.

Exposure Standards and Criteria. OSHA established exposure limits for several carcinogens categorized as combustion nuclei [i.e., benzo(a)pyrene, cadmium, nickel, benzene, n-nitrosodimethylamine]. These limits are established for industrial work environments and are not directly applicable to general indoor air situations. Underlying atherosclerotic heart disease may be exacerbated by carbon monoxide (CO) exposures.

Exposure Control Strategies. Exposure control strategies for combustion nuclei are similar in many ways to those for other particles. For combustion nuclei derived from space heating, air contamination can be avoided by proper installation and venting of equipment to ensure that these contaminants cannot enter the work or personal environment. Proper equipment maintenance is also essential to minimize exposures to combustion nuclei.

Exposures and Sources. In the nonindustrial indoor environment, particle concentrations are greatly affected by the outdoor environment. Diesel engines emit large quantities of fine particulate matter. Indoor particle sources may include cleaning, resuspension of particles from carpets and other surfaces, construction and renovation debris, paper dust, deteriorated insulation, office equipment, and combustion processes (including cooking stoves, fires, and environmental tobacco smoke).

Although asbestos is commonly found in buildings constructed before the 1970s, it generally does not represent a respiratory hazard except to individuals who actively disturb it during maintenance and construction.

An important source of particulates, environmental tobacco smoke (ETS) from cigarettes consists of exhaled mainstream smoke from the smoker and, with conventional cigarettes, the sidestream smoke emitted from the smoldering tobacco. Approximately 70 to 90% of ETS results from sidestream smoke, which has a chemical composition somewhat different from mainstream smoke. More than 4700 compounds have been identified in laboratory-based studies, including known human toxic and carcinogenic compounds such as carbon monoxide, ammonia, formaldehyde, nicotine, tobacco-specific nitrosamines, benzo(a)pyrene, benzene, cadmium, nickel, and aromatic amines. Many of these constituents are more concentrated in sidestream smoke than in mainstream smoke (Glantz and Parmley 1991). In studies conducted in residences and office buildings with tobacco smoking permitted, ETS was a substantial source of many gaseous and particulate PACs (Offermann et al. 1991).

Increased use of electronic cigarettes (e-cigarettes or e-cigs) and vaping has generated a new potential concern for indoor air quality. Data are still limited on potential exposures and human health risks posed by the use of e-cigarettes indoors, especially among bystanders from secondhand and third-hand exposures (AIHA 2014). Although the literature generally supports findings that e-cigarette emissions and exposure risks are much less harmful than tobacco smoke (AIHA 2014), emissions from these devices are not contaminant free. Nicotine is present in most forms of e-cigarettes, but the concentration can vary greatly and has also been found in some products identified as not containing nicotine (Burstyn 2013; Czogala et al. 2013; FDA 2009; Villa et al. 2012). Propylene glycol and vegetable glycerin are used as delivery vehicles for nicotine and various flavoring ingredients, which can break down into acrolein, formaldehyde, and acetaldehyde in the vapor (Geiss et al. 2014; Goniewicz et al. 2013; Lauterbach et al. 2012; Uchiyama et al. 2013). Flavorings used in e-cigarettes are typically considered safe for food or ingestion, but the health effects of inhaling them as vapors have not thoroughly been evaluated (AIHA 2014; Offerman 2014). Characterizing the differences in exposure from traditional cigarettes and from e-cigarettes is an active area of research.

Health Effects of Exposure. The health effects of exposure to combustion nuclei depend on many factors, including concentration, toxicity, and individual susceptibility or sensitivity to the particular substance. Combustion-generated PACs include many PAHs and nitro-PAHs that have been shown to be carcinogenic in animals (NAS 1983). Other PAHs are biologically active as tumor promoters and/or cocarcinogens. Mumford et al. (1987) reported high exposures to PAH and aza-arenes for a population in China with very high lung cancer rates.

According to the U.S. EPA (2005) fine particulate matter (particles less than 2.5 μm in diameter, or PM_2.5) is associated with lung disease, asthma, and other respiratory problems. Short-term exposure may cause shortness of breath, eye and lung irritation, nausea, light-headedness, and possible allergy aggravations.

PM_2.5 has been calculated to have the highest impact on health of studied chronic air pollutants inhaled in residences. The metric used was the disability-adjusted life years (DALYs). DALYs are a measure of the morbidity (disability) and mortality (death) caused by exposure to contaminants or other risks. PM_2.5 accounts for nearly 90% of the DALYs lost through chronic air pollutants inhaled in residences. Additional contaminants in descending importance ranked by DALYs are secondhand smoke (SHS), radon (for smokers), formaldehyde (a major source is composite wood products), and acrolein (a major source is cooking fats) (Logue et al. 2011, 2012). This type of analysis provides a rationale as well as a value that can be monetized to guide practitioners and researchers in determining which indoor contaminants are most important for control. From this analysis, PM_2.5 is clearly the obvious first target in indoor air quality: it is the dominant contaminant of concern in most residences, and one of the easiest and least expensive to control (primarily with filtration with higher-efficiency filters).

ETS has been shown to be causally associated with lung cancer in adults and respiratory infections, asthma exacerbations, middle ear effusion (DHHS 1986; NRC 1986), and low birth weight (Martin and Bracken 1986). The U.S. Environmental Protection Agency classifies ETS as a known human carcinogen (EPA 1992). Health effects can also include heart disease, headache, and irritation. ETS is also a cause of sensory irritation and annoyance (odors and eye irritation).

Exposure Standards. There are no established exposure guidelines for particles in nonindustrial indoor environments. The EPA’s National Ambient Air Quality standard (NAAQS) established primary and secondary standards for particle pollution. Primary standards provide public health protection, including protecting the health of sensitive populations such as asthmatics, children, and the elderly. Secondary standards provide public welfare protection, including protection against decreased visibility and damage to animals, crops, vegetation, and buildings. Table 3 gives information on primary and secondary standards for PM_2.5 and PM₁₀.

Exposure Control Strategies. Particulate or dust control strategies for the nonindustrial environment include source elimination or reduction, good housekeeping, general dilution ventilation, and upgraded filtration. In general, source control is preferred. Combustion appliances must be properly vented and maintained. If a dust problem exists, identify the type of dust to develop an appropriate intervention strategy. Damp dusting and high-efficiency vacuum cleaners may be considered. Building spaces under construction or renovation should be properly isolated from occupied spaces to limit transport of dust and other contaminants. Minimizing idling of diesel-powered vehicles near buildings can reduce entry of fine particulate matter.

Control of ETS has been accomplished primarily through regulatory mandates on the practice of tobacco smoking indoors. Most U.S. states and E.U. member states have passed laws to control tobacco smoking in at least some public places, including public buildings, restaurants, and workplaces, and the FAA (2000) has prohibited smoking on all flights to and from the United States, as have many airlines throughout the world. Where tobacco smoking is permitted, appropriate local and general dilution ventilation can be used for control; however, the efficacy of ventilation is unproven (Repace 1984). Some studies indicate that extremely high ventilation rates may be needed to dilute secondhand smoke to minimal risk levels (Repace and Lowrey 1985, 1993).

Bioaerosols are airborne biological particles derived from viruses, bacteria, fungi, protozoa, algae, mites, plants, insects, and their by-products, fragments, and cell mass components. Bioaerosols are present in both indoor and outdoor environments. For the indoor environment, locations that provide appropriate temperature and moisture conditions and a food source for biological growth may become problematic.

In microbiology, reservoirs allow microorganisms to survive, amplifiers allow them to proliferate, and disseminators effectively distribute bioaerosols. Building components and systems may have only one factor, or all three; for instance, a cooling tower is an ideal location for growth and dispersal of microbial contaminants and can be the reservoir, amplifier, and disseminator for Legionella (harboring microorganisms in scale, allowing them to proliferate, and generating an aerosol).

Both the physical and biological properties of bioaerosols need to be understood. For a microorganism to cause illness in building occupants, it must be transported in sufficient dose to a susceptible occupant. Airborne infectious particles behave physically in the same way as any other aerosol-containing particles with similar size, density, and electrostatic charge. The major difference is that bioaerosols may cause disease by several mechanisms (infection, allergic disease, immunomodulation, irritation, toxicosis), depending on the organism, dose, and susceptibility of the exposed population. Although microorganisms exist normally in indoor environments, the presence of abundant moisture and nutrients in interior spaces results in the growth of fungi, bacteria, protozoa, algae, or even nematodes (Arnow et al. 1978; Morey and Jenkins 1989; Morey et al. 1986; Strindehag et al. 1988). Thus, humidifiers, water spray systems, and wet porous surfaces can be reservoirs and sites for growth. Excessive air moisture (Burge 1995) and floods (Hodgson et al. 1985) can also result in proliferation of these microorganisms indoors. Turbulence associated with the start-up of air-handling unit plenums may also elevate concentrations of bacteria and fungi in occupied spaces (Buttner and Stetzenbach 1999; Yoshizawa et al. 1987).

Building Surface and Material Sources. Floors and floor coverings can be reservoirs for organisms that are subsequently resuspended into the air. Routine activity, including walking and vacuuming (Buttner et al. 2002), may even promote resuspension (Cox 1987). Some viruses may persist up to eight weeks on nonporous surfaces (Mbithi et al. 1991).

Building Water System Sources. Although potable water is usually delivered to buildings free of biological hazards, once the water enters the facility it becomes the responsibility of facility managers and owners to ensure that its microbial and chemical quality does not degrade. In fact, biological hazards associated with processes in building water systems cause considerable disease. Most cases of legionellosis, for example, result from exposure to potable water in buildings (McCoy 2005; WHO 2007).

Nonpotable water is a well-known source of infective agents and of noninfective biological particles. Baylor et al. (1977) demonstrated the sequestering of small particles by foam and their subsequent dispersal through bubble bursting. This dispersal may take place in surf, river sprays, or artificial sources such as whirlpools.

Building Occupant Sources. People are an important source of bacteria and viruses in indoor air. Infected humans can release virulent agents from skin lesions or disperse them by coughing, sneezing, or talking. Other means for direct release include sprays of saliva and respiratory secretions during dental and respiratory therapy procedures. Large droplets can transmit infectious particles to those close to the disseminator, and smaller particles can remain airborne for short or very long distances (Moser et al. 1979). Droplet nuclei can be transported over long distances, resulting in infection transmission, as shown by studies of SARS in Hong Kong (Li et al. 2005a, 2005b). Studies of student dorms found lower ventilation associated with higher incidence of infectious diseases (Sun et al. 2011).

Health Effects. The presence of microorganisms in indoor environments may cause infective and/or allergic building-related illnesses (Burge 1989; Morey and Feeley 1988). Some microorganisms under certain conditions may produce microbial volatile organic chemicals (MVOCs) (Hyppel 1984; Mason et al. 2010) that are malodorous. Microorganisms must remain viable to cause infection, although nonviable particles may promote an allergic disease, which is an immunological response. An organism that does not remain virulent in the airborne state cannot cause infection, regardless of how many units of organisms are deposited in the human respiratory tract. Virulence depends on factors such as relative humidity, temperature, oxygen, pollutants, ozone, and ultraviolet light (Burge 1995), each of which can affect survival and virulence differently for different microorganisms. Harmful chemicals and fragments produced by microorganisms can also cause irritant responses and carry biologically active metabolites (e.g., allergens, ligands) that trigger inflammatory immune responses (Drummond and Brown 2011; Green et al. 2005).

A wide variety of bacteria, fungi, and protozoa are prevalent in building water systems and can cause disease by transmission through water and air. Clinically important microorganisms known to cause disease in health care facilities include the bacteria Legionella, Pseudomonas, and Mycobacterium; the fungi Aspergillus and Fusarium; and the protozoa Cryptosporidium, Giardia, and Acanthamoeba.

Fungal Pathogens. Many fungal genera are widely distributed in nature and are common in the soil and on decaying vegetation, dust, and other organic debris (Levetin 1995). Fungi that have a filamentous structure are called molds, and reproduce by spores. Mold spores are small (2 to 10 μm in diameter), readily dispersed by water splash and air currents, and may remain airborne for long periods of time (Lighthart and Stetzenbach 1994; Streifel et al. 1989).

Dampness and mold growth/colonization in buildings have long been thought to cause increased health problems for occupants (Institute of Medicine 2004). In recent decades, multiple high-profile incidents have generated great public concern about mold in buildings, but also conflicting opinions on which health effects can be caused by dampness and mold, and on how to determine the level of risk in a building. Published reviews and meta-analyses of the scientific literature have clarified the available scientific basis for defining these health risks (Bornehag et al. 2001; Fisk et al. 2007, 2010; Institute of Medicine 2004; Kreiger et al. 2010; Mendell et al. 2011; WHO 2009).

Health studies have led to a consensus among health scientists that the presence in buildings of (1) visible water damage, (2) damp materials, (3) visible mold growth/colonization, or (4) mold odor indicates an increased risk of respiratory disease for occupants. In addition, evidence is accumulating that the more extensive, widespread, or severe these indicators, the greater the health risks. Known health risks include development of asthma, allergies, and respiratory infections; triggering of asthma attacks; and increased wheeze, cough, difficulty breathing, and other symptoms. Associations with other kinds of health effects have not been substantiated, but also have not been ruled out. Available information also suggests that children are more sensitive to dampness and mold than adults. The specific dampness-related agents that cause these respiratory health effects, whether molds, bacteria, other microbial agents, or dampness-related chemical emissions, have not been identified.

There also is consensus that the traditional methods used to measure molds in air or dust do not reliably predict increased health risks. Some newer methods of measuring mold, although promising, have not been proven to be better predictors of health effects than simply assessing the presence of evident dampness or mold growth/colonization. Therefore, current practices for the collection, analysis, and interpretation of environmental samples for mold-derived aerosols cannot be used to quantify health risks posed by dampness and mold growth/colonization in buildings or to guide health-based actions. Also, current consensus does not justify the differentiation of some molds as toxic or especially hazardous to healthy individuals. The only types of evidence that have been related consistently to adverse health effects are the presence of current or past water damage, damp materials, visible mold, and mold odor, not the number or type of mold spores or the presence of other markers of mold growth/colonization in indoor air or dust.

Bacterial Pathogens. Diseases produced by the bacterial genus Legionella are collectively called legionelloses. More than 45 species have been identified, with over 20 isolated from both environmental and clinical sources. Conditions favorable for Legionella spp. growth include water temperatures of 77 to 108°F; stagnant conditions; presence of scale, sediment, and biofilms; and the presence of amoebas (Geary 2000). Diseases produced by Legionella pneumophila include Legionnaires’ disease (pneumonia form) and Pontiac fever (flulike form). L. pneumophila serogroup 1 is the most frequently isolated from nature and most frequently associated with disease. Infection rates are affected by the strain of L. pneumophila as well as host condition (e.g., tobacco smoking, excessive weight, age). Legionellosis is not rare, but it is rarely diagnosed, and is severely underreported, often lost among other causes of pneumonia. McCoy (2006) estimated that, every day in the United States, an average of about 11 people die from legionellosis, and another 57 are infected but survive, often with lifelong debilitation.

In a review of waterborne infections from building water systems, it was estimated that 1400 deaths occur each year in the United States from Pseudomonas aeruginosa, another waterborne bacteria commonly found in building water systems (Anaissie et al. 2002).

Viral Pathogens. Outbreaks of infection in indoor air may also be caused by viruses. Viruses are readily disseminated from infected individuals, but cannot reproduce outside a host cell. Therefore, they do not reproduce in building structures or air-handling components, but can be distributed throughout buildings through duct systems and on air currents. Human-to-human dispersal is common. In one example, most of the passengers in an airline cabin developed influenza following exposure to one acutely ill person (Moser et al. 1979). In this case, the plane had been parked on a runway for several hours with the ventilation system turned off. Severe acute respiratory syndrome (SARS), caused by a corona virus similar to the common cold, was assumed to result from large droplet transmission; however, in an outbreak in a high-rise apartment, airborne transmission was the primary mode of disease spread, likely through dissemination from a bathroom drain (Yu et al. 2004). Ventilation and airflows in buildings were shown to affect the transmission of SARS in this outbreak and another outbreak in a hospital ward (Li et al. 2005a, 2005b).

Infectious diseases are transmitted through three primary routes: (1) direct contact and fomites (i.e., inanimate objects that transport infectious organisms from one individual to another), (2) large droplets [generally with a mass median aerodynamic diameter (MMAD) > 10 μm], and (3) fine particles, sometimes called droplet nuclei (MMAD < 10 μm) (Mandell et al. 1999). Routes of disease transmission that are not related to the environment or to buildings (e.g., blood-borne, insect vectored) exist, but are beyond the scope of this chapter. Table 4 lists infections considered transmissible by air.

Nonviable Biological Substances. Allergic reactions are an immunological response to foreign glycol proteins. The causes of the rapid increase in allergies all over the world are not known, but indoor exposures to new chemicals (e.g., plasticisers, flame retardants, biocides, cleaning products) and alterations to the gut microflora driving immunomodulation are suspected, as well as reduced ventilation. When a person has acquired an allergy, an acute attack may develop after dermal contact or inhalation of particles containing allergens (e.g., enzymes, mite and cockroach excreta, pet dander, pollen). The severity of immunological reactions to bioaerosols can vary dramatically, from discomfort (allergic rhinitis and sinusitis) to life-threatening asthma. Allergy testing in conjunction with a carefully obtained history may be helpful in identifying an offending agent. In cases of more severe illness, it may be necessary to remove an affected individual from exposure, even after appropriate abatement and exposure control methods have been instituted in the building, though this is the purview of the clinicians, and not of building professionals.

Exposure Guidelines for Bioaerosols. At present, numerical guidelines for bioaerosol exposure in indoor environments and for infectious pathogens that can spread via airborne routes are not available for the following reasons (Morey 1990):

Exposure Control Strategies. Because of the wide variety of pathogens and sources, a range of bioaerosol exposure control strategies may be required. Typically, these strategies should focus on source control (including good housekeeping and proper HVAC system operation and maintenance), but dilution ventilation, local exhaust ventilation, disinfection procedures, space pressure control, and filtration may also be considered.

Moisture control is the key to mold growth/colonization control. Molds need both food and water to survive; because molds can digest most things, water is the key factor that limits mold growth. The presence of water damage, dampness, visible mold, or mold odor in schools, workplaces, residences, and other indoor environments is unhealthy. It is not recommended to measure indoor microorganisms or the presence of specific microorganisms to attempt to determine the level of health hazard or the need for urgent remediation. Instead, address water damage, dampness, visible mold, and mold odor by (1) identifying and correcting the source of water that may allow microbial growth or contribute to other problems, (2) rapidly drying or removing damp materials, and (3) cleaning or removing mold colonies and mold-colonized (moldy) materials, as rapidly and safely as possible, to protect the health and well being of building occupants, especially children. More detailed information may be found in Harriman et al. (2001) and ASHRAE’s (2003) Mold and Moisture Management in Buildings.

ASHRAE Standard 188 and Guideline 12 provides environmental and operational guidance for safe operation of building water systems to minimize the risk of Legionnaires’ disease.

Exposures and Sources. In the industrial environment, a wide variety of gaseous contaminants may be emitted as process by-products (e.g., paints, solvents, and welding fumes) or as accidental spills and releases.

Health Effects of Industrial Exposures. Given that tens of thousands of contaminants are regularly used by industry, possible health effects can range from mild skin or eye irritation and headaches, to failure of major organs or systems and death.

Exposure standards and specific health effects for various industrial contaminants are discussed in the following section.

Exposure Standards. Occupational exposure standards or legal concentration limits are established by a country or by a widely recognized organization like the WHO, with specific clarifications or recommendations for each state, province, or territory. In the United States, the Occupational Safety and Health Administration (OSHA) sets permissible exposure limits (PELs) for toxic and hazardous substances, which are enforceable workplace regulatory standards. These are published yearly in the Code of Federal Regulations (29CFR1910, Subpart Z) and intermittently in the Federal Register. Most of the regulatory levels were derived from those recommended by the American Conference of Governmental Industrial Hygienists (ACGIH) and Agency for Toxic Substances and Disease Registry (ATSDR). The health effects on which these standards were based can be found in their publications. ACGIH reviews data on a regular basis and publishes annual revisions to their Threshold Limit Values (TLVs^®).

The National Institute for Occupational Safety and Health (NIOSH), a research agency of the U.S. Department of Health and Human Service, conducts research and makes recommendations to prevent work-related illness and injury. NIOSH publishes the Registry of Toxic Effects and Chemical Substances (RTECS), as well as numerous criteria on recommended standards for occupational exposures. Some compounds not listed by OSHA are covered by NIOSH, and their recommended exposure limits (RELs) are sometimes lower than the legal requirements set by OSHA. The NIOSH Pocket Guide to Chemical Hazards (NIOSH 2007) condenses these references and is a convenient reference for engineering purposes.

The harmful effects of gaseous pollutants depend on both short-term peak concentrations and the time-integrated exposures received by the person. OSHA defined three periods for concentration averaging and assigned allowable levels that may exist in these categories in workplaces for over 490 compounds, mostly gaseous contaminants. Abbreviations for concentrations for the three averaging periods are

The respective levels are presented in Tables Z-1, Z-2, and Z-3 of 29CFR1910.1000, Occupational safety and health standards: Air contaminants.

In non-OSHA literature, the AMP is sometimes called a short-term exposure limit (STEL), and a TWA8 is sometimes called a threshold limit value (TLV). NIOSH (1997) also lists values for the toxic limit that is immediately dangerous to life and health (IDLH).

Standards differ for industrial and nonindustrial environments (EHD 1987). A Canadian National Task Force developed guideline criteria for residential indoor environments (Health Canada 2010), and the World Health Organization (WHO) published indoor air quality guidelines for Europe (WHO 2010). Table 5 compares some of these guidelines with occupational criteria for selected contaminants.

Exposure Control Strategies. Gaseous contaminant control strategies include eliminating or reducing sources, local exhaust, general dilution ventilation, and using personal protective devices such as respirators. The most effective control strategy is source control. If source control is not possible, local exhaust ventilation can often be the most cost-effective method of controlling airborne contaminants. General dilution ventilation is often the least effective means of control. Ventilation and local exhaust for industrial environments are discussed more thoroughly in Chapters 31 and 32 of the 2019 ASHRAE Handbook—HVAC Applications.

Gaseous contaminants of concern in nonindustrial environments include organic compounds, refrigerants, and inorganic gases.

Volatile Organic Compounds.

Sources. Indoor sources of VOCs include building materials, furnishings, cleaning products, office and HVAC equipment, ETS [including products from e-cigarettes (vaping)], marijuana smoke, and people and their personal care products. Outdoor sources of VOCs may also enter the building through various airflow paths, including intake air and infiltration through the building envelope.

Health Effects. Potential adverse health effects of VOCs in nonindustrial indoor environments are not well understood, but may include (1) irritant effects, including perception of unpleasant odors, mucous membrane irritation, and exacerbation of asthma; (2) systemic effects, such as fatigue and difficulty concentrating; and (3) toxic, chronic effects, such as carcinogenicity (Girman 1989).

Chronic adverse health effects from VOC exposure are of concern because some VOCs commonly found in indoor air are human (benzene) or animal (chloroform, trichloroethylene, carbon tetrachloride, p-dichlorobenzene) carcinogens. Some other VOCs are also genotoxic. Theoretical risk assessment studies suggest that risk from chronic VOC exposures in residential indoor air is greater than that associated with exposure to VOCs in the outdoor air or in drinking water (McCann et al. 1987; Tancrede et al. 1987).

A biological model for acute human response to low levels of VOCs indoors is based on three mechanisms: sensory perception of the environment, weak inflammatory reactions, and environmental stress reaction (Mølhave 1991). A growing body of literature summarizes measurement techniques for the effects of VOCs on nasal (Koren 1990; Koren et al. 1992; Meggs 1994; Mølhave et al. 1993; Ohm et al. 1992) and ocular (Franck et al. 1993; Kjaergaard 1992; Kjaergaard et al. 1991) mucosa. It is not well known how different sensory receptions to VOCs are combined into perceived comfort and the sensation of air quality. This perception is apparently related to stimulation of the olfactory sense in the nasal cavity, the gustatory sense on the tongue, and the common chemical sense (Cain 1989; Mølhave 1991).

Cometto-Muñiz and Cain (1994a, 1994b) addressed the independent contribution of the trigeminal and olfactory nerves to the detection of airborne chemicals. Smell is experienced through olfactory nerve receptors in the nose. Nasal pungency, described as common chemical sensations such as prickling, irritation, tingling, freshness, stinging, and burning, is experienced through nonspecialized receptors of the trigeminal nerve in the face. Odor and pungency thresholds follow different patterns related to chemical concentration. Odor is often detected at much lower levels. A linear correlation between pungency thresholds of homologous series (of alcohols, acetates, ketones, and alkylbenzenes, all relatively nonreactive agents) suggests that nasal pungency relies on a physicochemical interaction with a susceptible biophase within the cell membrane. Through this nonspecific mechanism, low, subthreshold levels of a wide variety of VOCs, as found in many polluted indoor environments, may be additive in sensory impact to produce noticeable sensory irritation.

Exposure Standards. Few standards exist for exposure to VOCs in nonindustrial indoor environments. NIOSH, OSHA, and ACGIH have regulatory standards or recommended limits for industrial occupational exposures [ACGIH (annual); NIOSH 1992]. With few exceptions, concentrations observed in nonindustrial indoor environments fall well below (100 to 1000 times lower) published pollutant-specific occupational exposure limits. The California Office of Environmental Health Hazard Assessment (OEHHA 2016a) established chronic reference exposure limits (cRELs) for inhalation exposure to 80 compounds, including many VOCs found in indoor air, which can be used as guidelines for establishing appropriate IAQ criteria regarding specific VOCs of interest.

Total VOC (TVOC) concentrations were suggested as an indicator of the ability of combined VOC exposures to produce adverse health effects. This approach is no longer supported, because the irritant potential and toxicity of individual VOCs vary widely, and measured concentrations are highly dependent on the sampling and analytical methods used (Hodgson 1995). In controlled exposure experiments, odors become significant at roughly 3 mg/m³. At 5 mg/m³, objective effects were seen, in addition to subjective reports of irritation. Exposures for 50 min to 8 mg/m³ of synthetic mixtures of 22 VOCs led to significant irritation of mucous membranes in the eyes, nose, and throat (Kjærgaard et al. 1991).

Exposure Control Strategies. VOC control strategies include source elimination or reduction, local exhaust, air cleaning, and general dilution ventilation. Several emission testing standards [e.g., BIFMA Standard M7.1; CDPH (2010)] have been established to promote the use and production of low-VOC-emission materials and products. Air-cleaning technologies include physical and chemical adsorption, photocatalytic oxidization, and dynamic botanical filtration (Wang 2011). Caution is needed to ensure that target pollutants are sufficiently removed and no by-products with adverse health effects are produced (Pei and Zhang 2011; Zhang et al. 2011). Ventilation requirements and other means of control of gaseous contaminants are discussed more thoroughly in Chapter 16 of this volume and Chapter 46 of the 2019 ASHRAE Handbook—HVAC Applications.

Semivolatile organic compounds (SVOCs) include phthalates, alkylphenols, flame retardants, polycyclic aromatic hydrocarbons (PAHs), polychlorinated biphenyls (PCBs), and pesticides. Many SVOCs are associated with adverse health outcomes in laboratory animal studies and in some environmental epidemiology studies.

Sources. Indoor sources of SVOCs include consumer products and building materials such as detergents, toys, lotions, nail polish, perfume, cosmetics, shampoo, electronic equipment (e.g., computers, televisions), pesticides, furniture foam or stuffing, shower curtains, vinyl flooring, and PVC products. In general, since the 1950s, levels of volatile organic compounds (VOCs) increased and then decreased. During this same period, levels of SVOCs, such as those used as plasticizers and flame retardants, have increased and remain high (Rudel and Perovich 2009; Weschler 2009). Table 6 lists compounds representative of SVOCs encountered indoors (Weschler and Nazaroff 2008).

Health Effects. Exposures to SVOCs in nonindustrial indoor environments have been associated with adverse health effects in a number of recent studies. Exposures to these compounds have been linked to endocrine disruptions in both animals and in humans, poor semen quality (motility, number), birth abnormalities in anogenital distance, and premature sexual development (genital and reproductive anomalies such as hypospadias) (Hauser and Calafat 2005; Rogan and Ragan 2007; Swan 2008). Human exposure to SVOCs has also been studied by monitoring concentrations of metabolites in body fluids such as in urine or blood. Results show that people are exposed to multiple SVOCs everywhere, and that children often are more exposed than adults (EPA 2011). Biomonitoring data suggest that over 95% of the U.S. population is exposed to phthalates (Kato et al. 2004), and the body burden for polybrominated diphenyl ethers (PBDEs, used in flame retardants) in North Americans is 10 to 100 times higher than in Europeans because of the much higher indoor exposure of the U.S. population (Harrad et al. 2006; Sjodin et al. 2008).

When determining SVOC exposure pathways, remember that SVOCs can be either gaseous or condensed. They are redistributed from their original source to indoor air and subsequently to all interior surfaces, including airborne particles, settled dust, fixed surfaces, and human surfaces (Rudel and Perovich 2009; Weschler and Nazaroff 2008; Xu et al. 2010). Indeed, contaminated indoor environments have recently been recognized as a significant uptake pathway for SVOCs (Harrad et al. 2006; Xu et al. 2010). Exposure routes of SVOCs include diet, inhalation, dermal absorption, and oral ingestion of dust (Hauser and Calafat 2005; Weschler and Nazaroff 2008, 2012). Diet, the only pathway that is relatively insensitive to the indoor presence of SVOCs, is considered the dominant source for total intake (body burden) for many SVOCs. However, awareness is growing of potential exposure through inhalation, inadvertent ingestion, or skin adsorption (Hauser and Calafat 2005; Weschler and Nazaroff 2012). For some SVOCs, indoor exposures via these three pathways appear to be larger than that resulting from diet. Table 7 provides the indoor concentrations and body burden of selected semivolatile organic compounds.

Exposure Standards. Few standards exist for exposure to SVOCs in nonindustrial indoor environments. NIOSH, OSHA, EPA, and ACGIH have regulatory standards or recommended limits for industrial occupational exposures for inhalation, some of which are given in Table 5. The California Environmental Protection Agency’s Office of Environmental Health Hazard Assessment (OEHHA 2016b) maintains a list of VOCs and other chemicals known to the state to cause cancer or reproductive toxicity.

Lately, a new generation of scientific tools has emerged to rapidly measure responses from cells, tissues, and organisms following exposure to chemicals, including SVOCs. The goal of such methods is to rapidly screen and prioritize chemicals for more detailed toxicity testing (Judson et al. 2010). However, activities to compile exposure data to develop novel approaches and metrics to screen and evaluate chemicals based on biologically relevant human exposures are still in their initial stages.

Exposure Control Strategies. SVOC control strategies include source identification, elimination or reduction. Weschler and Nazaroff (2008) argued, based on theoretical considerations, that ventilation is not as effective in reducing indoor concentrations of SVOCs as it is in reducing indoor concentrations of VOCs. Although recent modeling studies indicate that ventilation has a limited ability to reduce indoor levels of most airborne SVOCs and thus the ability to reduce human exposures (Liang and Xu 2011; Xu et al. 2010), Weschler and Nazaroff (2008) showed that ventilation is generally ineffective in controlling human exposure because of the long-term persistence of condensed SVOCs. Laboratory studies have demonstrated the small impact that ventilation has on indoor airborne levels of di(2-ethylhexyl) phthalate (DEHP), a compound used as a plasticizer (Xu et al. 2010). Field studies are needed to evaluate the impact of ventilation on different types of SVOCs under realistic indoor conditions. Furthermore, there is also a lack of literature documenting SVOC exposure reductions via air cleaning. Table 7 shows indoor concentrations and body burdens of selected SVOCs.

Inorganic Gases.

Sources. Inorganic gases in the nonindustrial environment may come from a combination of outdoor air and indoor sources, including occupants (e.g., respiration, toiletries), processes (e.g., combustion, office equipment), and indoor air chemistry (e.g., reaction between ozone and alkenes).

Health Effects. Carbon monoxide is a chemical asphyxiant. Inhalation of CO causes a throbbing headache because hemoglobin has a greater affinity for CO than for oxygen (about 240 times greater), and because of a detrimental shift in the oxygen dissociation curve. Carbon monoxide inhibits oxygen transport in the blood by forming carboxyhemoglobin and inhibiting cytochrome oxidase at the cellular level. Cobb and Etzel (1991) suggested that CO poisoning at home represented a major preventable disease. Moolenaar et al. (1995) had similar findings, and suggested that motor vehicles and home furnaces were primary causes of mortality. Girman et al. (1998) identified both fatal outcomes and “episodes” and classed them by cause:

In a review of CO exposures in the United States from 2001 to 2003, the Centers for Disease Control (CDC 2005) found that nearly 500 people died and over 15,000 were treated in emergency departments each year after unintentional, non-fire-related CO exposures. Of cases with known sources, the most common source of CO was furnaces (18.5%), followed by motor vehicles (9.1%). Inappropriate use of portable generators, a growing problem, resulted in around 50 deaths per year from 2002 to 2005 (CPSC 2006).

Carbon dioxide can become dangerous not as a toxic agent but as a simple asphyxiant. When concentrations exceed 35,000 ppm, central breathing receptors are triggered and cause the sensation of shortness of breath. At progressively higher concentrations, central nervous system dysfunction begins because of displacement of oxygen. Measured concentrations of CO₂ in nonindustrial environments are typically below 1000 ppm, but can occasionally be as high as 2500 ppm, depending on occupant density and outdoor air ventilation rates (Persily 2015a). Nevertheless, much confusion exists regarding the significance of indoor CO₂ and its effects on occupant health and comfort (ASHRAE 2009).

Inhalation of nitric oxide (NO) causes methemoglobin formation, which adversely affects the body by interfering with oxygen transport at the cellular level. NO exposures of 3 ppm have been compared to carbon monoxide exposures of 10 to 15 ppm (Case et al. 1979, in EPA 1991).

Nitrogen dioxide (NO₂) is a corrosive gas with a pungent odor, with a reported odor threshold between 0.11 and 0.22 ppm. NO₂ has low water solubility, and is therefore inhaled into the deep lung, where it causes a delayed inflammatory response. Increased airway resistance has been reported at 1.5 to 2 ppm (Bascom 1996). NO₂ is reported to be a potential carcinogen through free radical production (Burgess and Crutchfield 1995). At high concentrations, NO₂ causes lung damage directly by its oxidant properties, and may cause health effects indirectly by increasing host susceptibility to respiratory infections. Health effects from exposures to ambient outdoor concentrations or in residential situations are inconsistent, especially in studies relating to exposures from gas cooking stoves (Samet et al. 1987). Indoor concentrations of NO₂ often exceed ambient concentrations because of the presence of strong indoor sources and a trend toward more energy-efficient (tighter) homes. Acute toxicity is seldom seen from NO₂ produced by unvented indoor combustion, because insufficient quantities of NO₂ are produced. Chronic pulmonary effects from exposure to combinations of low-level combustion pollutants are possible, however (Bascom et al. 1996).

Sulfur dioxide (SO₂) is a colorless gas with a pungent odor detected at about 0.5 ppm (EPA 1991). Because SO₂ is quite soluble in water, it readily reacts with moisture in the respiratory tract to irritate the upper respiratory mucosa. Concomitant exposure to fine particles, an individual’s depth and rate of breathing, and preexisting disease can influence the degree of response to SO₂ exposure.

Ozone (O₃) is a pulmonary irritant and has been known to alter human pulmonary function at concentrations of approximately 0.12 ppm (Bates 1989). However, inhaling ozone at considerably lower concentrations (e.g., about 0.080 ppm) has been shown to decrease respiratory function in healthy children (Spektor et al. 1988a). Outdoor ozone levels as low as 0.020 ppm have been shown to increase mortality, and levels below 0.010 ppm may be required for safety (ASHRAE 2011). These levels are far below current federal NAAQS levels of 0.075 ppm. Reducing ozone levels indoors to as low as reasonably achievable (ALARA) levels by various means is recommended.

Products of ozone reactions are often more irritating than precursors. Ozone and isoprene react to form free radicals, formaldehyde, methacrolein, and methyl vinyl ketone. Ozone and terpenoids react to form free radicals, secondary ozonides, formaldehyde, acrolein, hydrogen peroxide, organic peroxides, dicarbonyls, carboxylic acids, and submicron particles.

Ozone reacts with many organic chemicals and airborne particulate matter commonly found indoors. Weschler (2006) summarizes current knowledge of these reactions and their products, which include both stable reaction products that may be more irritating than their chemical precursors (Mølhave et al. 2005; Tamas et al. 2006; Weschler and Shields 2000) and relatively short-lived products that are highly irritating and may also have chronic toxicity or carcinogenicity (Destaillats et al. 2006; Nazaroff et al. 2006; Weschler 2000; Wilkins et al. 2001; Wolkoff et al. 2000).

Chen et al. (2012) assessed the influence of indoor exposure to outdoor ozone on short-term mortality in U.S. communities. When air with ozone passes through loaded filters, the downstream concentrations of submicron-sized particles is higher than the upstream concentration. Ozone removal efficiencies on used filters change by one of at least two different removal mechanisms: reactions with compounds on the filter media after manufacturing, and reactions with compounds on captured particles (Beko et al. 2007).

The scientific literature is well developed in showing the effect of ozone on respiratory function and health effects of exposure to elevated levels of ozone (Lippmann 1993; Spektor et al. 1988b, 1991; Thurston et al. 1997). A critical review of the health effects of ozone is provided by Lippmann (1989).

Exposure to ozone at 0.060 to 0.080 ppm causes inflammation, bronchoconstriction, and increased airway responsiveness. The EPA’s BASE study of over 100 randomly selected typical U.S. office buildings (Apte et al. 2007) found a clear statistical relationship between ambient ozone concentrations and building-related health symptoms, despite the fact that only one building had a workday average ambient ozone concentration greater than the then-current 8 h national ambient air quality standards [NAAQS; see EPA (2016a)] level of 0.080 ppm.

Ambient air ozone concentrations down to 0.020 ppm are associated with increased mortality (Bell et al. 2005). Several researchers have explored the relationship between ozone and mortality (Bates 2005; Goodman 2005; Ito et al. 2005; Levy et al. 2005).

Although ozone uptake (deposition velocity v_d) on diverse materials varies greatly (e.g., from 0.025 m/h for aluminum to 28 m/h for gypsum board), uptakes in a wide variety of building types and occupancies are within a fairly narrow range (between 0.9 and 1.5 m/h).

Inhalation exposures to gaseous oxides of nitrogen (NO_x), sulfur (SO₂), and ozone (O₃) occur in residential and commercial buildings. These air pollutants are of considerable concern because of the potential for acute and chronic respiratory tract health effects in exposed individuals, particularly individuals with preexisting pulmonary disease.

Exposure Standards and Guidelines. Currently, there are no specific U.S. government standards for nonindustrial occupational exposures to air contaminants. Occupational exposure criteria are health based; that is, they consider only healthy workers, and not necessarily individuals who may be unusually responsive to the effects of chemical exposures. The U.S. EPA’s (2016a) NAAQS are also health-based standards designed to protect the general public from the effects of hazardous airborne pollutants (see Chapter 11). Table 8 is not meant as a health-based guideline for evaluating indoor exposures to inorganic gases; rather, it is intended for comparison and consideration by investigators of the indoor environment. These criteria may not be completely protective for all occupants.

Exposure Control Strategies. Inorganic gas contaminant control strategies include source elimination or reduction, local exhaust, space pressure control, general dilution ventilation, and gaseous air cleaning. Ventilation requirements and other means of control of gaseous contaminants are discussed more thoroughly in Chapter 16 of this volume and Chapter 46 of the 2019 ASHRAE Handbook—HVAC Applications.

The by-products of indoor air chemistry can be limited by using carbon-based filters in locations where outdoor ozone concentrations commonly approach or exceed the NAAQS.

Environmental conditions for good thermal comfort minimize effort of the physiological control system. The control system regulates internal body temperature by varying the amount of blood flowing to different skin areas, thus increasing or decreasing heat loss to the environment. Additional physiological response includes secreting sweat, which can evaporate from the skin in warm or hot environments, or increasing the body’s rate of metabolic heat production by shivering in the cold. For a resting person wearing trousers and a long-sleeved shirt, thermal comfort in a steady state is experienced in a still-air environment at 75°F. A zone of comfort extends about 3°F above and below this optimum level (Fanger 1970).

An individual can minimize the need for physiological (involuntary) responses to the thermal environment, which generally are perceived as uncomfortable, in various ways. In a cool or cold environment, these responses include increased clothing, increased activity, or seeking or creating an environment that is warmer. In a warm or hot environment, the amount of clothing or level of physical activity can be reduced, or an environment that is more conducive to increased heat loss can be created. Some human responses to the thermal environment are shown in Figure 1.

Figure 1. Related Human Sensory, Physiological, and Health Responses for Prolonged Exposure

Cardiovascular and other diseases and aging can reduce the capacity or ability of physiological processes to maintain internal body temperature through balancing heat gains and losses. Thus, some people are less able to deal with thermal challenges and deviations from comfortable conditions. Metabolic heat production tends to decrease with age, as a result of decreasing basal metabolism together with decreased physical activity. Metabolic heat production at age 80 is about 20% less than that at age 20, for comparable size and mass. People in their eighties, therefore, may prefer an environmental temperature about 3°F warmer than people in their twenties. Older people may have reduced capacity to secrete sweat and to increase their skin blood flow, and are therefore more likely to experience greater strain in warm and hot conditions, as well as in cool and cold conditions. However, the effect of age on metabolism and other factors related to thermal response varies considerably from person to person, and care should be taken in applying these generalizations to specific individuals.

Hypothermia is defined as a core body temperature of less than 95°F. Hypothermia can result from environmental cold exposure, but may also be induced by other conditions, such as metabolic disorders and drug use. Occupational hypothermia occurs in workers in a cold environment when heat balance cannot be met while maintaining work performance. Elderly persons sitting inactive in a cool room may become hypothermic, because they often fail to observe a slow fall in body temperature (Nordic Conference on Cold 1991).

Deleterious effects of cold on work performance derive from peripheral vasoconstriction and cooling, which slows down the rate of nerve conduction and muscle contraction, and increases stiffness in tendons and connective tissues. This induces clumsiness and increases risk for injury (e.g., in occupational settings). Direct effects of cold include injuries from frostbite (skin freezes at 32 to 35.5°F) and a condition called immersion foot, in which the feet are exposed to wetness and temperatures of 34 to 50°F for more than 12 h, and vasoconstriction and low oxygen supply lead to edema and tissue damage.

In hyperthermia, body temperatures are above normal. A deep-body temperature increase of 4°F above normal does not generally impair body function. For example, it is not unusual for runners to have rectal temperatures of 104°F after a long race. An elevated body temperature increases metabolism. However, when body temperature increases above normal for reasons other than exercise, heat illness may develop. Heat illness represents a number of disorders from mild to fatal, which do not depend only on the hyperthermia in itself. In heat stroke, the most severe condition, the heat balance regulation system collapses, resulting in a rapid rise in body temperature. Central nervous system function deteriorates at deep body temperatures above 106 to 108°F. Convulsions may occur above such temperatures, and cells may be damaged. This condition is particularly dangerous for the brain, because lost neurons are not replaced. Thermoregulatory functions of sweating and peripheral vasodilation cease at about 110°F, after which body temperatures tend to rise rapidly if external cooling is not imposed (Blatteis 1998; Hales et al. 1996).

Ordinary seasonal changes in temperate climates are temporally associated with illness. Many acute and several chronic diseases vary in frequency or severity with time of year, and some are present only in certain seasons. Most countries report increased mortality from cardiovascular disease during colder winter months. Minor respiratory infections, such as colds and sore throats, occur mainly in fall and winter. More serious infections, such as pneumonia, have a somewhat shorter season in winter. Intestinal infections, such as dysentery and typhoid fever, are more prevalent in summer. Diseases transmitted by insects, such as encephalitis and endemic typhus, are limited to summer, because insects are active in warm temperatures only.

Hryhorczuk et al. (1992), Martinez et al. (1989), and others describe a correlation between weather and seasonal illnesses, but correlations do not necessarily establish a causal relationship. Daily or weekly mortality and heat stress in heat waves have a strong physiological basis directly linked to outdoor temperature. In indoor environments, which have well-controlled temperature and humidity, such temperature extremes and the possible adverse effects on health are strongly attenuated.

Impacts to human health can include the direct effects of climate change such as increased ambient temperatures, air pollution, and extreme weather. Additionally, indirect impacts of climate change may include vector-borne diseases and expanded habitats, industrial transitions, emerging industries (e.g., renewable energy, carbon sequestration, “green industries,” toxic waste from PV cell fabrication, noise and flickering from wind turbines), increased use of pesticides, and changes in the built environment (Institute of Medicine 2014; NIOSH 2014).

In general, climate change can affect people from these perspectives:

The role of weather-induced ambient temperature extremes in producing discomfort, incapacity, and death has been studied extensively (Katayama and Momiyana-Sakamoto 1970). Military personnel, deep-mine workers, and other workers occupationally exposed to extremes of high and low temperature have been studied, but the importance of thermal stress affecting both the sick and healthy general population is not sufficiently appreciated. Collins and Lehmann (1953) studied weekly deaths over many years in large U.S. cities and demonstrated the effect of heat waves in producing conspicuous periods of excess mortality. Excess mortality caused by heat waves was of the same amplitude as that from influenza epidemics, but tended to last one week instead of the four to six weeks of influenza epidemics.

Ellis (1972) reviewed heat wave-related excess mortality in the United States. Mortality increases of 30% over background are common, especially in heat waves early in the summer. Much of the increase occurs in the population over age 65, more of it in women than in men, and many deaths are from cardiovascular, cerebrovascular, or respiratory causes (often exacerbated preexisting conditions). Oeschli and Buechley (1970) studied heat-related deaths in Los Angeles heat waves of 1939, 1955, and 1963. Kilbourne et al. (1982) suggested that the same risk factors (i.e., age, low income, and African-American derivation) persist in more recent heat death epidemics.

Among the most notable lethal heat waves in Europe are Athens in 1987 and 1988 (Giles et al. 1990), Seville in 1988 (Diaz et al. 2002), Valencia in 1991 and 1993 (Ballester et al. 1997), London in 1995 (Hajat et al. 2002), the Netherlands between 1979 and 1991 (Kunst et al. 1993), and Paris in 2003 (Thirion et al. 2005). In the 2003 Parisian heat wave, about 3000 people died.

The temperature/mortality relation varies greatly by latitude and climatic zone (McMichael et al. 2006). Occupants of hotter cities are more affected by colder temperatures, and occupants of colder cities are more affected by warmer temperatures. People living in urban environments are at greater risk than those in nonurban regions. Thermally inefficient housing and the so-called urban heat island effect amplify and extend the rise in temperatures (especially overnight).

Figure 2. Isotherms for Comfort, Discomfort, Physiological Strain, Effective Temperature (ET*), and Heat Stroke Danger Threshold

Hardy (1971) showed the relationship of health data to comfort on a psychrometric diagram (Figure 2). The diagram contains ASHRAE effective temperature (ET*) lines and lines of constant skin moisture level or skin wettedness. Skin wettedness is defined as that fraction of the skin covered with water to account for the observed evaporation rate. The ET* lines are loci of constant physiological strain, and also correspond to constant levels of physiological discomfort (i.e., slightly uncomfortable, comfortable, and very comfortable) (Gonzalez et al. 1978). Skin wettedness, as an indicator of strain (Berglund and Cunningham 1986; Berglund and Gonzalez 1977) and the fraction of the skin wet with perspiration, is fairly constant along an ET* line. Numerically, ET* is the equivalent temperature at 50% rh that produces the strain and discomfort of the actual condition. The summer comfort range is between an ET* of 73 and 79°F. In this region, skin wettedness is less than 0.2. Heat strokes occur generally when ET* exceeds 93°F (Bridger and Helfand 1968). Thus, the ET* line of 95°F is generally considered dangerous. At this point, skin wettedness will be 0.4 or higher.

The dots in Figure 2 correspond to heat stroke deaths of healthy male U.S. soldiers assigned to sedentary duties in midwestern army camp offices (Shickele 1947). Older people can be expected to respond less well to thermal challenges than do healthy soldiers. This was apparently the case in the Illinois heat wave study (Bridger and Helfand 1968), where the first wave with a 33% increase in death rate and an ET* of 85°F affected mainly the over-65-year-old group. The studies suggest that the “danger line” represents a threshold of significant risk for young healthy people, and that the danger tends to move to lower values of ET* with increasing age.

Cardiovascular diseases are largely responsible for excess mortality during heat waves. For example, Burch and DePasquale (1962) found that heart disease patients with decompensation (i.e., inadequate circulation) were extremely sensitive to high temperatures, and particularly to moist heat. However, both cold and hot temperature extremes have been associated with increased coronary heart disease deaths and anginal symptoms (Teng and Heyer 1955).

Both acute and chronic respiratory diseases often increase in frequency and severity during extreme cold weather. No increase in these diseases has been noted in extreme heat. Additional studies of hospital admissions for acute respiratory illness show a negative correlation with temperature after removal of seasonal trends (Holland 1961). Symptoms of chronic respiratory disease (bronchitis, emphysema) increase in cold weather, probably because reflex constriction of the bronchi adds to the obstruction already present. Greenberg (1964) found evidence of cold sensitivity in asthmatics: emergency room treatments for asthma increased abruptly in local hospitals with early and severe autumn cold spells. Later cold waves with even lower temperatures produced no such effects, and years without early extreme cold had no asthma epidemics of this type. Patients with cystic fibrosis are extremely sensitive to heat because their reduced sweat gland function greatly diminishes their ability to cope with increased temperature (Kessler and Anderson 1951).

Itching and chapping of the skin are influenced by (1) atmospheric factors, particularly cold and dry air; (2) frequent washing or wetting of skin; and (3) low indoor humidities. Although skin itching is usually a winter cold-climate illness in the general population, it can be caused by excessive summer air conditioning (Gaul and Underwood 1952; Susskind and Ishihara 1965).

People suffering from chronic illness (e.g., heart disease) or serious acute illnesses that require hospitalization often manage to avoid serious thermal stress. Katayama and Momiyana-Sakamoto (1970) found that countries with the most carefully regulated indoor climates (e.g., Scandinavian countries, the United States) have only small seasonal fluctuations in mortality, whereas countries with less space heating and cooling exhibit greater seasonal swings in mortality. For example, mandatory air conditioning in retirement and assisted living homes in the southwest United States has virtually eliminated previously observed mortality increases during heat waves.

The skin has cold, warm, and pain sensors to feed back thermal information about surface contacts. When the skin temperature rises above 113°F or falls below about 59°F, sensations from the skin’s warm and cold receptors are replaced by those from pain receptors to warn of imminent thermal injury to tissue. The rate of change of skin temperature and not just the actual skin temperature may also be important in pain perception. Skin temperature and its rate of change depend on the temperature of the contact surface, its conductivity, and contact time. Table 9 gives approximate temperature limits to avoid pain and injury when contacting three classes of conductors for various contact times (ISO Standard 13732-1).

Vibration in a building originates from both outside and inside the building. Outdoor sources include blasting operations, road traffic, overhead aircraft, underground railways, earth movements, and weather conditions. Indoor sources include doors closing, foot traffic, moving machinery, elevators, escalators, HVAC systems, and other building services. Vibration is an omnipresent, integral part of the built environment. The effects of vibration on building occupants depend on whether it is perceived by those persons and on factors related to the building, building location, occupants’ activities, and perceived source and magnitude of vibration. Factors influencing the acceptability of building vibration are presented in Figure 3.

The combination of hearing, seeing, or feeling vibration determines human response. Components concerned with hearing and seeing are part of the visual environment of a room and can be assessed as such. The perception of mechanical vibration by feeling is generally through the cutaneous and kinesthetic senses at high frequencies, and through the vestibular and visceral senses at low frequencies. Because of this and the nature of vibration sources and building responses, building vibration may be conveniently considered in two categories: low-frequency vibrations less than 1 Hz and high-frequency vibrations of 1 to 80 Hz.

Figure 3. Factors Affecting Acceptability of Building Vibration

Measurement and Assessment. Human response to vibration depends on vibration of the body. The main vibrational characteristics are vibration level, frequency, axis (and area of the body), and exposure time. A root-mean-square (RMS) averaging procedure over the time of interest is often used to represent vibration acceleration (ft/s² · RMS). Vibration frequency is measured in cycles per second (Hz), and the vibration axis is usually considered in three orthogonal, human-centered translational directions: up-and-down, side-to-side, and fore-and-aft. Although the coordinate system is centered inside the body, in practice, vibration is measured at the human surface, and measurements are directly compared with relevant limit values or other data concerning human response.

Rotational motions of a building in roll, pitch, and yaw are usually about an axis of rotation some distance from the building occupants. For most purposes, these motions can be considered as the translational motions of the person. For example, a roll motion in a building about an axis of rotation some distance from a seated person has a similar effect as side-to-side translational motions of that person, etc.

Most methods assess building vibrations with RMS averaging and frequency analysis. However, human response is related to the time-varying characteristics of vibration as well. For example, many stimuli are transient, such as those caused by a train passing a building. The vibration event builds to a peak, followed by a decay in level over a total period of about 10 s. The nature of the time-varying event and how often it occurs during a day are important factors that might be overlooked if data are treated as steady-state and continuous.

Low-Frequency Motion (1 Hz). The most commonly experienced form of slow vibration in buildings is building sway. This motion can be alarming to occupants if there is fear of building damage or injury. Whereas occupants of two-story wood frame houses accept occasional creaks and motion from wind storms or a passing heavy vehicle, such events are not as accepted by occupants of high-rise buildings. Detected motion in tall buildings can cause discomfort and alarm. The perception thresholds of normal, sensitive humans to low-frequency horizontal motion are given in Figure 4 (Chen and Robertson 1972; ISO Standard 6897). The frequency range is from 0.06 to 1 Hz or, conversely, for oscillations with periods of 1 to 17 s. The natural frequency of sway of the Empire State Building in New York City, for example, has a period of 8.3 s (Davenport 1988). The thresholds are expressed in terms of relative acceleration, which is the actual acceleration divided by the standard acceleration of gravity g (32.2 ft/s²). The perception threshold to sway in terms of building accelerations decreases with increasing frequency and ranges from 0.16 to 0.06 ft/s².

Figure 4. Acceleration Perception Thresholds and Acceptability Limits for Horizontal Oscillations

For tall buildings, the highest horizontal accelerations generally occur near the top at the building’s natural frequency of oscillation. Other parts of the building may have high accelerations at multiples of the natural frequency. Tall buildings always oscillate at their natural frequency, but the deflection is small and the motion undetectable. In general, short buildings have a higher natural frequency of vibration than taller ones. However, strong wind forces energize the oscillation and increase the horizontal deflection, speed, and accelerations of the structure.

ISO Standard 6897 states that building motions should not produce alarm and adverse comment from more than 2% of the building’s occupants. The level of alarm depends on the interval between events. If noticeable building sway occurs for at least 10 min at intervals of 5 years or more, the acceptable acceleration limit is higher than if this sway occurs annually (Figure 4). For annual intervals, the acceptable limit is only slightly above the normal person’s threshold of perception. Motion at the 5-year limit level is estimated to cause 12% to complain if it occurred annually. The recommended limits are for purely horizontal motion; rotational oscillations, wind noise, and/or visual cues of the building’s motion exaggerate the sensation of motion, and, for such factors, the acceleration limit is lower.

Figure 5. Median Perception Thresholds to Horizontal (Solid Lines) and Vertical (Dashed Line) Vibrations

The upper line in Figure 4 is intended for offshore fixed structures such as oil drilling platforms. The line indicates the level of horizontal acceleration above which routine tasks by experienced personnel would be difficult to accomplish on the structure. Because they are routinely in motion in three dimensions, Figure 4 does not apply to transportation vehicles.

High-Frequency Motion (1 to 80 Hz). Higher-frequency vibrations in buildings are caused by machinery, elevators, foot traffic, fans, pumps, and HVAC equipment. Further, the steel structures of modern buildings are good transmitters of high-frequency vibrations. Sensitivity to these higher-frequency vibrations is indicated in Figure 5 (data from Parsons and Griffin 1988), showing median perception thresholds to vertical and horizontal vibrations in the 2 to 100 Hz frequency range. The average perception threshold for vibrations of this type is from 0.03 to 0.3 ft/s², depending on frequency and on whether the person is standing, sitting, or lying down.

People detect horizontal vibrations at lower acceleration levels when lying down than when standing. However, a soft bed decouples and isolates a person fairly well from vibrations of the structure. The threshold to vertical vibrations is nearly constant at approximately 0.04 ft/s² for both sitting and standing positions from 2 to 100 Hz. This agrees with observations by Reiher and Meister (1931).

Many building spaces with critical work areas (surgery, precision laboratory work) are considered unacceptable if vibration is perceived by the occupants. In other situations and activities, perceived vibration may be acceptable. Parsons and Griffin (1988) found that accelerations twice the threshold level were unacceptable to occupants in their homes. A method of assessing acceptability in buildings is to compare the vibration with perception threshold values (Table 10).

In general terms, sound transmitted through air consists of oscillations in pressure above and below ambient atmospheric pressure. A vibrating object causes high- and low-pressure areas to be formed; these areas propagate away from the source. The entire mechanical energy spectrum includes infrasound and ultrasound as well as audible sound (Figure 6).

Health Effects. Hearing loss is generally considered the most undesirable effect of noise exposure, although there are other effects. Tinnitus, a ringing in the ears, is really the hearing of sounds that do not exist. It often accompanies hearing loss. Paracusis is a disorder where a sound is heard incorrectly; that is, a tone is heard, but has an inappropriate pitch. Speech misperception occurs when an individual mistakenly hears one sound for another (e.g., when the sound for t is heard as a p).

Figure 6. Mechanical Energy Spectrum

Hearing loss can be categorized as conductive, sensory, or neural. Conductive hearing loss results from a general decrease in the amount of sound transmitted to the inner ear. Excessive ear wax, a ruptured eardrum, fluid in the middle ear, or missing elements of bone structures in the middle ear are all associated with conductive hearing loss. These are generally not occupationally related and are generally reversible by medical or surgical means. Sensory hearing losses are associated with irreversible damage to the inner ear. Sensory hearing loss is further classified as (1) presbycusis, loss caused as the result of aging; (2) noise-induced hearing loss (industrial hearing loss and sociacusis, which is caused by noise in everyday life); and (3) nosoacusis, losses attributed to all other causes. Neural deficits are related to damage to higher centers of the auditory system.

Noise-induced hearing loss is believed to occur in the most sensitive individuals among those exposed for 8 h per day over a working lifetime at levels of 75 dBA, and for most people similarly exposed to 85 dBA.

Even when below levels that can cause adverse health effects, sound and noise can lead to reduced indoor environmental quality and potentially other unhealthy situations. For example, people often react to noisy mechanical equipment by shutting the equipment off or blocking openings that provide a transmission pathway for the noise. Shutting off ventilation systems can lead to unhealthy indoor environments. Blocking some openings, such as those designed to provide combustion air, can also cause problems. Therefore, selecting components that are unlikely to lead to occupant dissatisfaction can be important in providing good indoor environmental quality.

Figure 7. Electromagnetic Spectrum

For methods to address potential sound and noise problems, see Chapter 48 of the 2019 ASHRAE Handbook—HVAC Applications.

Ionizing radiation is the part of the electromagnetic spectrum with very short wavelengths and high frequencies, and it has the ability to ionize matter. These ionizations tend to be very damaging to living matter. Background radiation that occurs naturally in the environment is from cosmic rays and naturally occurring radionuclides. It has not been established whether exposure at the low dose rate of average background levels is harmful to humans.

The basic standards for permissible air concentrations of radioactive materials are those of the National Committee on Radiation Protection, published by the National Bureau of Standards as Handbook 69 (NBS 1969). Industries operating under licenses from the U.S. Nuclear Regulatory Commission or state licensing agencies must meet requirements of the Code of Federal Regulations, Title 10, Part 20. Some states have additional requirements.

An important naturally occurring radionuclide is radon (²²²Rn), a decay product of uranium in the soil (²³⁸U). Radon is chemically inert. Details of units of measurement, typical radon levels, measurement methods and control strategies can be found in Chapter 11.

Health Effects of Radon. Radon is the leading cause of lung cancer among nonsmokers, according to EPA (2016b) estimates. Most information about radon’s health risks comes from studies of workers in uranium and other underground mines. The radioactive decay of radon produces a series of radioactive isotopes of polonium, bismuth, and lead. Unlike their chemically inert radon parent, these progeny are chemically active and can attach to airborne particles that subsequently deposit in the lung, or deposit directly in the lung without attachment to particles. Some of these progeny, like radon, are alpha-particle emitters, which can cause cellular changes that may initiate lung cancer when they pass through lung cells (Samet 1989). Thus, adverse health effects associated with radon are caused by exposures to radon decay products, and the amount of risk is assumed to be directly related to the total exposure. Even though it is the radon progeny that present the possibility of adverse health risks, radon itself is usually measured and used as a surrogate for progeny measurements because of the expense involved in accurate measurements of radon progeny.

Exposure Standards. Many countries have established standards for exposure to radon. Some international action levels are listed in Table 12.

About 6% of U.S. homes (i.e., 5.8 million homes) have annual average radon concentrations exceeding 148 Bq/m³ (4 pCi/L), approaching the action level (150 Bq/m³) set by the U.S. Environmental Protection Agency (Marcinowski et al. 1994). Because there is no known safe level of exposure to radon, the EPA (2016b) also recommends that all homes be tested for radon, regardless of geographic location, and remedial measures be considered in homes with radon levels between 2 and 4 pCi/L.

Ultraviolet radiation, visible light, and infrared radiation are components of sunlight and of all artificial light sources. Microwave and radio-frequency radiation are essential in a wide range of communication technologies and are also in widespread use for heating as in microwave ovens and heat sealers, and for heat treatments of various products. Power frequency fields are an essential and unavoidable consequence of the generation, transmission, distribution, and use of electrical power.

Optical Radiation. Ultraviolet (UV), visible, and infrared (IR) radiation compose the optical radiation region of the electromagnetic spectrum. The wavelengths range from 100 nm in the UV to 1 mm in the IR, with 100 nm generally considered to be the boundary between ionizing and nonionizing. UV wavelengths range from 100 to 400 nm, visible from 400 to 760 nm, and IR from 760 nm to 1 mm.

Optical radiation can interact with a medium by reflection, absorption, or transmission. The skin and eyes are the organs at risk in humans. Optical radiation from any spectral region can cause acute and/or chronic biologic effects given appropriate energy characteristics and exposure. These effects include tanning, burning (erythema), premature “aging,” and skin cancer; and dryness, irritation, cataracts, and blindness in the eyes.

The region of the electromagnetic spectrum visible to humans is known as light. There can be biological, behavioral, psychological, and health effects from exposure to light. Assessment of these effects depends on the purpose and application of the illumination. Individual susceptibility varies, with other environmental factors (air quality, noise, chemical exposures, and diet) acting as modifiers. It is difficult, therefore, to generalize potential hazards. Light pollution is the presence of unwanted light.

Light penetrating the retina not only allows the exterior world to be seen, but, like food and water, is also used in a variety of metabolic processes. Darkness stimulates the pineal gland to secrete melatonin, which regulates the human biological clock. This, in turn, influences reproductive cycles, sleeping, eating patterns, activity levels, and moods. The color of light affects the way the objects appear. Distortion of color rendition may result in disorientation, headache, dizziness, nausea, and fatigue.

As the daylight shortens, the human body may experience a gradual slowing down, loss of energy, and a need for more sleep. It becomes harder to get to work, and depression or even withdrawal may take place. This type of seasonal depression, brought on by changes in light duration and intensity, is called seasonal affective disorder (SAD). Sufferers also complain of anxiety, irritability, headache, weight gain, and lack of concentration and motivation. This problem is treated through manipulation of environmental lighting (exposure to full-spectrum lighting for extended periods, 12 h/day).

Radio-Frequency Radiation. Just as the body absorbs infrared and light energy, which can affect thermal balance, it can also absorb other longer-wavelength electromagnetic radiation. For comparison, visible light has wavelengths in the range 0.4 to 0.7 μm and infrared from 0.7 to 10 μm, whereas the wavelength of K and X band radar is 12 and 28.6 mm. The wavelength of radiation in a typical microwave oven is 120 mm. Infrared is absorbed within 1 mm of the surface (Murray 1995).

Figure 8. Maximum Permissible Levels of Radio Frequency Radiation for Human Exposure (Adapted from ANSI/IEEE Standard C95.1-2005)

The heat of absorbed radiation raises skin temperature and, if sufficient, is detected by the skin’s thermoreceptors, warning the person of possible thermal danger. With increasing wavelength, radiation penetrates deeper into the body. Energy can thus be deposited well beneath the skin’s thermoreceptors, making the person less able or slower to detect and be warned of the radiation (Justesen et al. 1982). Physiologically, these longer waves only heat the tissue and, because the heat may be deeper and less detectable, the maximum power density of such waves in occupied areas is regulated (ANSI Standard C95.1) (Figure 8). Maximum allowed power densities are less than half of sensory threshold values.