Pulmonary Medicine

Indoor and Outdoor Air Pollution

What every physician needs to know:

Exposure to indoor and outdoor air pollutants may cause and/or exacerbate respiratory and other system diseases and may increase the population’s risk for morbidity and mortality from malignant and nonmalignant diseases. Air pollution exposure may also cause sensory irritation and decrease well-being through, for example, loss of visibility.

Although air pollution has probably had adverse effects on health throughout history though natural occurrences, such as volcanic eruptions, industrialization and electric power generation brought new sources of pollution--including localized sources, such as power plants, and sometimes immense emissions of combustion byproducts, particles, nitrogen oxides, and sulfur oxides--into adjacent areas where people lived and worked. During the twentieth century, cars, trucks, and other fossil-fueled vehicles created “smog,” or photochemical pollution, first recognized in the Los Angeles Basin in the 1940s.

The unprecedented growth of some urban areas that has formed “megacities” like Mexico City, Sao Paulo, and Shanghai has led to unrelenting air pollution from massive fleets of vehicles and snarled traffic and from polluting industries and power plants. Rarely, there are also tragic events, such as the collapse of the two towers of the World Trade Center that resulted in clouds of dense air pollution.

There has also been increasing recognition that the problem of air pollution extends to indoor environments. In low-income countries, exposure to smoke from biomass fuel combustion is widespread and is typically at high concentrations, as it has been for centuries. In high-income countries, indoor pollutants are generated by human activities and are released from the materials used for construction and furnishings. These indoor pollutants are often maintained at unhealthful concentrations by building designs that seal them in because of limited exchange of indoor air with outdoor air.

Several factors related to specific pollutant characteristics and patterns of exposure determine the likelihood of injury from inhalation of indoor or outdoor air pollutants.

Pollutant Characteristics

Uptake of gases: Penetration into and retention within the respiratory tract of gaseous pollutants vary widely, depending on the physical properties of the gas (e.g., solubility), the concentration of the gas in the inspired air, the rate and depth of ventilation, and the extent to which the material is reactive.

Highly water- soluble gases, such as formaldehyde and SO2, are almost completely extracted in the upper airways. Removal of less water-soluble gases like NO2 and O3 is much less complete, and these gases may penetrate to the distal airways and alveoli. Exercise greatly augments penetration of gases into the deep lung and the total dose of pollutants delivered to the airways.

Particle deposition and retention: Deposition depends on several factors, including the particles' aerodynamic properties (primarily particle size), airway anatomy, and breathing pattern. Particles larger than 10 μm in aerodynamic diameter are filtered out in the nose and nasopharynx, while particles smaller than 10 μm tend to be deposited in the tracheobronchial tree. Deposition in the alveoli is maximal for particles smaller than 1-2 um in diameter, while particles smaller than 100 nanometers (ultrafine particles) can deposit throughout the respiratory tract. Removal of particles from the larger airways occurs by the mucociliary apparatus within hours of deposition. Clearance from the deep lung by alveolar macrophages is much slower, requiring days to months.

Personal Exposure

Definitions of concentration, exposure, and dose are fundamental to considering the health effects of air pollution. Concentration is the amount of material present in the air. For the respiratory tract, exposure is the amount of time spent in contaminated air; exposure is given the units of concentration x time. Dose is the amount of material that enters the body. A biologically effective dose is the amount of material that must reach the target site, such as the alveoli, for injury to occur. Total personal exposure is the relevant index of exposure, which refers to the time-weighted average pollutant concentration in the microenvironment in which a person spends time. For example, for exposure to particles, an important microenvironment might include an office in which smoking is permitted.

Studies of time-activity patterns indicate that residents of most high-income countries spend most of their time indoors, so personal exposure to many pollutants takes place indoors. Data on time use in a number of countries showed that people spend an average of 65-75 percent of their time inside their homes and more than 90 percent of their time indoors. Even so, time spent outdoors may be the predominant determinant of exposure for some pollutants, such as ozone, especially for people who exercise outdoors and receive an augmented dose of ozone to their lungs because of the increased ventilation caused by exercising.

Exposure to indoor and outdoor air pollutants may cause and/or exacerbate respiratory and other system diseases and may increase the population’s risk for morbidity and mortality from malignant and nonmalignant diseases. Pollution exposure may also cause sensory irritation and decrease well-being through, for example, loss of visibility.

Although air pollution has probably had adverse effects on health throughout history through natural occurrences, such as volcanic eruptions, industrialization and electric power generation brought new sources of pollution--including localized sources, such as power plants, and sometimes immense emissions of combustion byproducts, particles, nitrogen oxides, and sulfur oxides--into adjacent areas where people lived and worked.

During the twentieth century, cars, trucks, and other fossil-fueled vehicles created “smog,” or photochemical pollution, first recognized in the Los Angeles Basin in the 1940s. The unprecedented growth of some urban areas that has formed “megacities” like Mexico City, Sao Paulo, and Shanghai has led to unrelenting air pollution from massive fleets of vehicles and snarled traffic and from polluting industries and power plants. Rarely, there are also tragic events, such as the collapse of the two towers of the World Trade Center that resulted in clouds of very dense air pollution.

Classification:

Outdoor air is polluted with a dynamic mixture of pollutants from both natural and manmade sources. The nature of the mixture depends primarily on the mix of sources and their operations and on meteorology. The mixture includes primary pollutants like nitrogen oxides and primary particles, which come directly from their sources, and secondary pollutants like ozone and secondary particles, which are formed through chemical and physical transformations. These pollutants are variably classified based on their characteristics and sources. One commonly used classification in the United States is based on Section 108 of the Clean Air Act, which covers “criteria pollutants” (particulate matter, ozone, nitrogen dioxide, sulfur dioxide, carbon monoxide, and lead) and toxic air pollutants and lists 189 pollutants, including carcinogens and irritants.

For public health and particularly for persons who have respiratory and cardiovascular disease, exposure to particulate matter and ozone at levels associated with adverse health effects is common. Particulate matter in urban air is typically a heterogeneous mixture with three size ranges: the ultrafine range (less than 0.10 microns in aerodynamic diameter), the fine range (less than 2.5 microns in aerodynamic diameter), and the coarse range (between 2.5 and 10 microns in aerodynamic diameter). The ultrafine particles, which reflect fresh combustion, are in highest numbers near roadways, where they come from vehicles, while most of the mass in the fine range is secondary particles. The coarse mode particles in urban areas are comprised of dust, tire debris, bioaerosols, and other materials.

Ozone is an indicator of oxidant pollution formed through sunlight-driven photochemistry that involves nitrogen oxides and hydrocarbons. Concentrations vary across the day based on traffic, sunlight, and weather. First identified in Los Angeles, photochemical pollution now affects much of the United States.

For both inhaled particles and ozone, oxidative injury with local and systemic consequences is considered to be the key mechanism of injury. Particulate matter in urban air typically has carcinogens among its components. Decades of epidemiological research link these air pollutants to adverse respiratory effects, including exacerbation of the chronic lung diseases, asthma and COPD. At very high concentrations of particulate matter, excess deaths have been well documented, particularly among those who suffer from chronic heart or lung disease. Epidemiological studies document increased short- and long-term mortality associated with particulate matter at levels present over the last several decades. A large literature links particulate matter to adverse cardiovascular effects as well.

As for ozone, acute but reversible reduction of lung function is well documented from experimental exposures, and epidemiological evidence shows exacerbation of asthma and possible impact on mortality at current concentrations.

There are myriad forms and sources of pollutants indoors, including combustion (tobacco smoking, stoves, fireplaces, and wood stoves), household products, construction materials, biological agents (e.g., microbes and pets), off-gassing from water, and soil gas, the origin of most indoor radon. These agents affect health and cause disease through diverse mechanisms, inflammation and irritation, immune responses, carcinogenesis, and effects on the central nervous system. Therefore, the spectrum of adverse respiratory consequences is broad and includes upper airway symptoms, causation and exacerbation of asthma, hypersensitivity pneumonitis, and lung cancer.

A large number of potential toxicants exist in the indoor environment (Figure 1), and several have been well characterized and described extensively in the literature. Representative examples of agents associated with acute or chronic toxicity from inhalation include wood smoke, biological agents, radon, second-hand cigarette smoke, and formaldehyde.

Occupational and Environmental Disorders with Borders

Wood Smoke

Environmental Sources of Exposure

Wood smoke is a complex mixture in terms of both physical and chemical characteristics and in its toxicological properties. Available data for developed countries suggest that the routine operation of a properly installed and maintained wood stove or the entrance of outdoor air contaminated with the wood smoke of neighbors does not greatly affect indoor air quality. By contrast, in developing countries, biomass fuel combustion for cooking and space heating can lead to very high exposure to indoor toxicants.

Mechanism of Injury

The toxicology of some components of wood smoke, such as benzo[a]pyrene, other polycyclic organic compounds, and nitrogen oxides, has been well studied. These components can produce inflammation and oxidant injury and can act as carcinogens. By contrast, the toxicology and mechanism of injury from wood smoke as a complex mixture is not well studied or understood.

Spectrum of Respiratory Disorders Associated with Exposure

Most of the epidemiology on the health effects of wood smoke is derived from studies in developing countries, where intense smoke exposure results from the use of cooking fires in poorly ventilated dwellings. Several studies indicate increases in acute respiratory illnesses, asthma, and chronic respiratory morbidity in children, COPD in women who have never smoked, and chronic respiratory morbidity in adults from exposure to wood smoke.

Biological Agents

Environmental Sources of Exposure

Indoor allergens and microbes, the principal biological agents in indoor air pollution that are relevant to human health, have diverse sources. Some of the most severe and prevalent indoor biological pollution arises from the growth of microorganisms or mold on interior surfaces that are wet or moist. Indoor levels of allergens and microbes may be increased by accumulation of materials like human or animal dander and growth of fungi and bacteria on interior surfaces or in air conditioning systems. Other common indoor allergens include those from house dust mites and cockroaches. Indoor pollen derived almost entirely from outdoor plants, and fungus spores from outdoors may also enter the indoor environment in air infiltration systems or on people, animals, or objects that move from outdoors to indoors.

Mechanism of Injury

Biological agents cause upper and lower respiratory infections, immunologic responses, and inflammation. Although considerable attention has focused on the effects of allergic responses to fungi, these micro-organisms also cause non-allergic responses. Some species of fungi, including some molds, are capable of producing mycotoxins and volatile and semi-volatile compounds, and they may cause a “toxic syndrome.” Non-allergic responses that may occur include neurotoxicity, immunotoxicity, sensory irritation, and dermal toxicity.

Spectrum of Respiratory Disorders Associated with Exposure

A wide spectrum of disease has been associated with biological agents. Bacteria may result in upper or lower respiratory infections that range from acute bronchitis to pneumonia. Hypersensitivity pneumonitis, asthma symptoms, increased bronchial reactivity, and lower respiratory illnesses have been linked with mold and damp indoor environments. Allergy-type symptoms or worsening of asthma symptoms may occur as a result of exposure to common indoor allergens.

Radon

Environmental Sources of Exposure

Radon, a colorless and odorless gas, originates from the decay of naturally occurring uranium-238. Present in soil gas, it enters homes through openings in basements and around foundations, drawn in by the pressure gradient that a structure creates across the ground. The concentration depends on the local geology, including the porosity of the earth and the concentration of radium, the precursor of radon. In some places, radon may also be present in high concentrations in water and off-gassed during use of water. Radon is also a well-documented occupational carcinogen that causes lung cancer. Underground mines can be contaminated by very high concentrations of radon, as in uranium mines.

Mechanism of Injury

Radon decays into a series of particulate radioactive progeny, two of which are alpha-particle-emitting polonium isotopes. Alpha particles, which have high mass and high energy, can create ionization tracks across cells that damage DNA. Therefore, lung cancer caused by radon is attributed to the traversal of basal cells in the respiratory epithelium by alpha particles emitted by the polonium progeny that have been deposited in the airways. Evidence in support of this mechanism comes from biophysical principles and experimental data. Because the energy of the alpha particles does not depend on concentration, the risk of lung cancer associated with radon varies directly with the exposure; there is no threshold below which there is no risk.

Spectrum of Respiratory Disorders Associated with Exposure

Risk for lung cancer is the sole consequence of concern for the general population exposed to radon. However, in heavily exposed underground miners, there is some indication that radon exposure contributes to fibrosis; it has also been examined as a cause of non-respiratory cancers but findings have been inconsistent. The epidemiological evidence shows that radon causes lung cancer in both those who smoke and those who have never smoked, and there is evidence of a synergy between smoking and radon in causing lung cancer. Radon has not been definitively linked to any particular histological type of lung cancer; observations in underground uranium miners showed that the first excess cases following exposure had an unexpectedly high frequency of small-cell carcinoma.

Secondhand Cigarette Smoke

Environmental Sources of Exposure

Secondhand smoke (SHS) refers to the mixture of diluted sidestream cigarette smoke and exhaled mainstream smoke that is inhaled by nonsmokers in contaminated indoor environments. SHS is a complex and dynamic mixture of gaseous and particulate components that changes as it is diluted and various chemical transformations occur. The concentration of SHS depends on the number of smokers in the room and their pattern of smoking, on the level of exchange of the indoor air with outdoor air, and on removal mechanisms, including surface deposition and filtration. In modern buildings with central air-handling units, SHS from one space may be distributed to others.

Mechanism of Injury

SHS is a rich mixture that includes agents that can cause symptoms and disease through diverse mechanisms, including irritation, inflammation, and carcinogenesis. For example, SHS includes many agents that have been classified as carcinogenic by the World Health Organization’s International Agency for Research on Cancer (IARC), along with oxidant species that can contribute to carcinogenesis through non-specific mechanisms.

Spectrum of Respiratory Disorders Associated with Exposure

Diverse respiratory effects have been linked to SHS exposure in children and adults. The first epidemiological studies on SHS, carried out in the 1960s and 1970s, were directed at lower respiratory illnesses in infants and young children. Subsequently, a lengthy list of adverse effects of SHS exposure in children has been identified, including risk of lower respiratory illnesses and middle-ear problems, exacerbation and possibly causation of asthma, and reduced lung function growth. In 1981, reports of two epidemiological studies showed increased risk for lung cancer associated with SHS in those who had never smoked. Now both lung cancer and coronary heart disease are causally associated with SHS in those who have never smoked. SHS is also a well-established cause of eye and upper-airway irritation.

Formaldehyde

Environmental Sources of Exposure

Formaldehyde is a natural product in some foods, and it is naturally present in the human body as a metabolic intermediate. However, it is a widely used chemical and a component of many materials used in homes and furnishings. (It is also a component of SHS.) Formaldehyde has been a particular concern in several indoor environments where high concentrations have been documented: homes insulated with improperly cured urea-formaldehyde foam insulation (UFFI) and in poorly ventilated mobile homes and trailers with formaldehyde-emitting particle board and plywood. It is also present in outdoor air, where major emission sources include power plants, incinerators, refineries, manufacturing facilities, and automobiles.

Mechanism of Injury

Formaldehyde has a simple one-carbon chemical structure and has been linked to both non-malignant and malignant health outcomes. For non-malignant effects associated with inhaled formaldehyde, key mechanisms include triggering of irritant receptors and non-specific inflammation. For carcinogenesis in the respiratory tract, two mechanisms may be relevant: genotoxicity and for nasal tumors, a mode of action characterized by regenerative cellular proliferation resulting from cytotoxicity.

Spectrum of Respiratory Disorders Associated with Exposure

Diverse respiratory effects have been investigated in relation to inhaled formaldehyde. Of these, irritation is a well-established consequence. The evidence is less certain for other respiratory outcomes, including reduction of lung function and causation and exacerbation of asthma. In workers who have high levels of exposure, formaldehyde exposure has been linked to cancers of the nose, nasal cavity, and nasopharynx.

Are you sure your patient has had exposure to indoor or outdoor air pollutants? What should you expect to find?

With few exceptions (e.g., hypersensitivity pneumonitis and carbon monoxide poisoning) air pollution does not cause “signature” diseases. Rather, air pollution contributes to the general burden of respiratory diseases, making contributions that are significant from the public health perspective. Risk assessment methods are used to calculate the contributions of various pollutants to the public health burden. These estimates address population-level effects but are not informative as to which individuals have been harmed by air pollution. For example, indoor radon is estimated to be the second leading cause of lung cancer in the United States, contributing to about 20,000 deaths annually.

One syndrome, “sick-building syndrome,” has been associated with indoor environments that are unhealthy because of indoor pollution, temperature, humidity, and other factors. Respiratory symptoms may be a component of the non-specific picture of sick-building syndrome, which is diagnosed on the basis of symptomatology and the temporal link of its occurrence to presence in the triggering environment.

Beware: there are other diseases that can mimic exposure to indoor or outdoor air pollutants.

Not applicable.

How and/or why did the patient develop a condition related to indoor or outdoor air pollutants?

Not applicable.

Which individuals are at greatest risk of developing a condition related to indoor and outdoor air pollution?

Air pollution exposures vary by place and time. In the United States, the Environmental Protection Agency, the states, and the municipalities carry out extensive monitoring of the key pollutants, particularly the criteria pollutants. Not surprisingly, these data show that levels are highest in major urban areas, and fine-scale studies show that exposures can be particularly intense alongside major roadways. Individuals who are likely to have higher exposures tend to live in inner cities and to live close to industrial sources. Because people who live in these areas tend to be of lower socioeconomic status, they are also more likely to have lower quality housing and to have higher exposures to indoor air pollution. The term “vulnerability” has been used to refer to this potential for higher exposures, while "environmental inequity" or "environmental injustice" refers to the higher exposures for those who are less advantaged.

By contrast, susceptibility refers to a higher risk for developing disease or other adverse outcomes at a particular exposure than that of those who are not susceptible. Broad groups considered as susceptible include infants and the elderly, persons with chronic heart or lung diseases, and those with other chronic diseases, such as diabetes. Research is in the process of addressing genetic determinants of susceptibility.

What laboratory studies should you order to help make the diagnosis, and how should you interpret the results?

Few lab tests are specifically relevant, with the exception of tests for exposures that have specific biomarkers: carboxyhemoglobin for CO, blood lead level, and antibody screens for hypersensitivity pneumonitis. As for exposure to tobacco smoke in indoor air, the level of cotinine, a nicotine metabolite, can be measured in saliva, blood, and urine, but this measurement is largely made for research purposes.

While not a “lab test,” inexpensive, passive devices can readily measure indoor concentration of radon with reasonable accuracy. The Environmental Protection Agency recommends measurement of indoor radon for most homes and in some jurisdictions, and it has become required with the sale of a house.

What imaging studies will be helpful in making or excluding the diagnosis?

Not applicable.

What non-invasive pulmonary diagnostic studies will be helpful in making or excluding the diagnosis of a condition related to indoor or outdoor air pollution?

Although pulmonary function tests may document obstructive, restrictive and mixed patterns following exposure to high levels of pollutants, such tests are generally not useful in detecting adverse effects in specific individuals exposed to ambient levels of pollution.

What diagnostic procedures will be helpful in making or excluding the diagnosis?

Not applicable.

What pathology/cytology/genetic studies will be helpful in making or excluding the diagnosis?

Not applicable

If you decide the patient has a condition related to indoor or outdoor air pollution, how should the patient be managed?

Controlling the health effects of indoor and outdoor air pollution requires strategies oriented toward both populations as a whole and individual patients.

Patient-oriented Strategies

Modifying time-activity patterns to limit time outside during episodes of pollution represents the most effective strategy. Those susceptible to air pollution should stay indoors during pollution episodes. During air pollution events, affected individuals should discontinue vigorous exercise outdoors, as exercise increases the dose of pollution delivered to the respiratory tract.

Use of medication should follow the usual clinical indications, and therapeutic regimens should not be adjusted because of the occurrence of a pollution episode without evidence of an adverse effect on symptoms or function.

Under most circumstances, health care providers should not recommend respiratory protection as a method for reducing the risks of ambient air pollution. Similarly, under most circumstances, health care providers should not recommend air cleaners as a method for reducing the risks of ambient air pollution or cleaning of air ducts in the home, as they have not been shown to have health benefits.

Community-oriented Strategies

The EPA developed an Air Quality Index (AQI) that provides descriptors of air quality and guidelines for cautionary statements. The actions taken when “alert levels” are reached or anticipated include issuing public health advisories. The EPA’s recommendations are used by local air pollution agencies in preparing daily air quality summaries to be disseminated to the media.

Pulmonologists may be faced with community issues that range from building-related issues to the effects of local sources, such as power plants and manufacturing facilities. Exposure to environmental pollutants may disproportionately affect disadvantaged communities, and the term “environmental justice” is used in addressing inequities between poorer and more well-to-do communities. Since these inequities are often complex issues that exceed the expertise of the local physician, guidance from public health and environmental agencies should be sought.

What is the prognosis for patients managed in the recommended ways?

Not applicable.

What other considerations exist for patients?

Not applicable

What’s the evidence?

http://www.atsdr.cdc.gov/toxprofiles/index.asp.

"What constitutes an adverse health effect of air pollution? Official statement of the American Thoracic Society ". Am J Resp Crit Care Med. vol. 161. 2000. pp. 665-673.

"HEI Panel on the Health Effects of Traffic-Related Air Pollution. Traffic-related air pollution: A critical review of the literature on emissions, exposure, and health effects. HEI Special Report 17". Health Effects Institute. 2010.

"Institute of Medicine, Committee on Indoor Spaces and Health: Damp indoor spaces and health". National Academy Press. 2004.

Samet, JM, Dominici, F, Curriero, FC, Coursac, I, Zeger, SL. "Fine particulate air pollution and mortality in 20 U.S.cities, 1987–1994.". NEJM. vol. 343. 2000. pp. 1742-1749.

Samet, JM, Geyh, A, Utell, MJ. "The legacy of the World Trade Center dust". N Engl J Med. vol. 356. 2007. pp. 2233-2236.

Samet, JM, Utell, MJ, A.P. Fishman, J.A, Elias, J. A, Fishman, M.A, Grippi, R.M. "Indoor and outdoor air pollution". Fishman’s pulmonary diseases and disorders. McGraw-Hill. 2008. pp. 1009-1036.

Spengler, JD, Samet, JM, McCarthy, JF. "Indoor Air Quality Handbook". McGraw-Hill. 2001.

Straif, K, Cohen, A, Samet, JM. "IARC Scientific Publication No. 161: Air Pollution and Cancer". International Agency for Research on Cancer. 2013.

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