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Indoor air pollution: acute adverse health effects and host susceptibility.

Introduction

Indoor air contains a complex mixture of chemical, biological, and physical pollutants, or agents. Depending on factors such as pollutant concentration and sensitivity of occupants, exposure to these pollutants may result in a number of adverse health effects. Understanding the pathogenic mechanisms underlying these effects, and thus identifying populations particularly susceptible to them, can help reduce uncertainty in establishing guidelines and allow pollution prevention efforts to focus on those agents with the greatest potential to cause harm.

This paper reviews common indoor air agents and considers currently available evidence for mechanisms of acute health effects. Susceptible populations are identified, and others are proposed, based on recognized mechanisms of the health effects. As the discussion is limited to acute health effects, illnesses with long latency periods have been excluded, such as asbestosis and lung cancer caused by radon.

Research efforts to identify mechanisms of injury and thus populations susceptible to low-level indoor air pollutants are illustrative of the changing perspective of public health and air pollution. Table 1 shows that when researchers and agencies concerned with public health devote more attention to air indoors, where average Americans spend 90 percent of their time (2), emphasis shifts from single-pollutant exposures to low-level exposures to multiple agents.

Air Pollutants and the Indoor Environment

Indoor environmental pollutants may be broadly categorized as biological agents, gases, particulates, and chemicals. Biological agents include proteins from dust mites, insects, and pets (hide, urine, fecal droppings); molds and mildew; infectious agents; and pollen. Building material may contribute agents from wood, wall coverings, carpeting, sealants, fiberglass, paints, and resins. Combustion sources such as stoves and automobiles contribute gases such as carbon dioxide and nitrogen dioxide. Cleaning solutions, perfumes, and insecticides are other sources of indoor air agents that may affect the health of occupants.

Experts often link increased indoor air pollution problems to tighter building construction beginning in the 1970s with the "energy crisis." In addition to the trend toward tighter building construction, many of the components used for buildings have changed over the years, with more emphasis on synthetic plastics and polymers in favor of "natural" materials such as granite and wood. The development of new sealants, caulks, and other building materials has also presented additional sources of volatile organic compounds, as such compounds may be emitted by these substances.
TABLE 1


Air Pollution: Shifting Emphasis in Public Health Concern and
Research (I).


From To


Outdoor air and occupational Indoor air and nonoccupational
exposures exposures


Cancer effects Noncancer effects


High levels of single Multiple pollutants at low levels
pollutants


Avoidance of clinical disease Protection of the general public
in highly exposed individuals from disease at lower exposures;
 attempt to protect even the most
 sensitive individuals


As a result of these factors and personal lifestyle choices, the air we breathe in our homes, office buildings, and other indoor spaces may contain any number of airborne agents capable of exerting adverse health effects. This paper considers some of the more common agents, their health effects, and individual susceptibility to the materials.

Acute Health Effects and Mechanisms of Action

Exposure to agents in indoor air may result in allergic reaction, irritation and other toxic effects, or infection. Occupants may experience irritation of the nasal and respiratory tract mucosa, allergic reactions, skin complaints, and general symptoms, including the difficulty concentrating often reported in sick building syndrome, or multiple chemical sensitivity.

Indoor air pollutants may exert their effects through allergic mechanisms, nonallergic mechanisms, or both. Mechanisms of allergic reactions may be classified as antibody or cell-mediated, and grouped into four categories. Nonallergic mechanisms of action may involve sensory irritation (nerve reflex), infection, and cytotoxic effects (via alterations in normal biochemistry or physiology). A brief discussion of both allergic and nonallergic mechanisms is provided below. To assist in the presentation of concepts, Table 2 provides an explanation of terms which have very specific meanings but are used as general descriptions in discussions of mechanisms or health effects.

Allergic Mechanisms

Allergic reactions result from an adverse response of the immune system to environmental agents. Allergic reactions involving the respiratory system may evoke asthma, rhinitis (runny nose), eye irritation, sneezing, and nasal congestion. In immediate (Type I) hypersensitivity, IgE and IgG antibodies bind to receptors on mast cells and basophils. If the antibody molecule then binds antigen, pharmacologically active amines, such as histamine, are released from the mediator cell (e.g., mast cell, basophil). These mediators result in vasodilation, edema, and generation of an inflammatory response. These responses tend to occur quickly after exposure to an antigen to which the individual has been sensitized. Allergic rhinitis and asthma induced by dust mites is an example of the Type I reaction.

The cytolytic or Type II reactions can be mediated by both IgG and IgM antibodies. These reactions are usually attributed to the antibody's ability to fix complement (a series of plasma proteins), opsonize particles, or function in an antibody-dependent cellular cytotoxicity reaction.

The Type III, or Arthus reactions are mainly mediated by IgG through a mechanism involving the generation of antigen-antibody complexes [TABULAR DATA FOR TABLE 3 OMITTED] that subsequently fix complement. The complexes become deposited in the vascular endothelium, where a destructive inflammatory response occurs. This is contrasted with the Type II reaction, where the inflammatory response is induced by antibodies directed against the tissue antigens. Trimellitic anhydride, a chemical widely used in the manufacture of plastics, may induce Type II and III hypersensitivity responses.

Delayed hypersensitivity, or Type IV responses are not mediated by antibodies but rather by macrophages and sensitized T lymphocytes. When these T lymphocytes come in contact with the sensitizing antigen, an inflammatory reaction is generated. Lymphokines are produced, followed by an influx of granulocytes and macrophages. Delayed hypersensitivity is one of the mechanisms implicated in reactions to isocyanates, a class of reactive chemicals.

Indirect immune effects occur when exposure to air pollutants either suppresses or enhances the immune response to other material. Dependent upon the concentration, sulfur dioxide, ozone, and nitrogen dioxide have been shown to either enhance or suppress the response of the respiratory system to inhaled foreign materials in laboratory animals. To date, however, this effect has not been demonstrated in humans (3).

Nonallergic Mechanisms

Nonallergic mechanisms may be broadly categorized as irritation, cytotoxicity, and infection. Irritation involves a reflex response of the respiratory system due to stimulation of nerve endings. Nitrogen dioxide is a widely recognized respiratory tract irritant.

Cytotoxicity may occur through alterations in normal cellular biochemistry and physiology and includes interference with receptors, membrane functions, and cellular energy production; binding to biomolecules; and selective cell loss. As an example, carbon monoxide both interferes with transport proteins and interferes with cellular energy production by binding to the reduced form of iron in hemoglobin and blocking oxygen delivery to tissues. As another example, lipid peroxidation is a proposed mechanism of toxicity from nitrogen dioxide and ozone. Chemical stimulation of the olfactory-hypothalamic-limbic pathway in the brain is one mechanism proposed for the symptoms associated with multiple chemical sensitivity. To date, no experimental proof has been provided in support of this idea (4).

Virus and bacteria present indoors are capable of causing infection. The most readily recognized infectious disease attributed to indoor air spaces is caused by Legionella (Legionnaire's Disease).

Some agents may act via multiple mechanisms and may be responsible for more than one type of symptom. Additionally, inhalation of certain agents may produce symptoms of disease that mimic immunological syndromes but are not immunologically mediated. Chemicals such as formaldehyde produce a pseudoallergic reaction that resembles immediate hypersensitivity, although demonstrable antibody is not detectable. Irritation of mucosal surfaces may stimulate protective responses (e.g., sneezing, coughing, and tearing) that appear superficially to be immunological in nature but are related to the stimulation of epithelial irritant receptors by chemicals.

Susceptible Populations

Individuals exposed to the same concentration of the same agent may respond differently. Individuals may be more sensitive or susceptible as a result of exaggerated exposure (such as through exercise), some innate predisposing trait, life-style, or the universal factor of age. Individuals especially sensitive or susceptible to certain adverse effects have been identified for some indoor air pollutants. As research continues to elucidate the mechanisms by which air pollutants cause injury, factors which contribute to differences in susceptibility will be identified. These sensitive groups may be the target populations for indoor air quality guidelines just as populations sensitive to air pollutants are recognized and protected by air quality standards of the U.S. Clean Air Act.

The elderly and those with impaired health (especially reduced cardiopulmonary function) are examples of broad population groups generally considered to be especially susceptible to adverse health effects from air pollution. Because of their greater activity and because of developing lungs, children may also be more susceptible to adverse effects of indoor air pollutants. Peak expiratory flow rates (PEFRs) are lower in children due to age and body/lung size, which may affect the rate at which inhaled agents are cleared from the lungs (5).

The airways of asthmatics are more responsive to a variety of stimuli. Therefore, these individuals may have lower thresholds to pollutant gases or particles than do healthy, nonasthmatic subjects.

In other individuals, genetic determinants may influence the circulating levels of antiproteases or antioxidants in the blood, components which protect against inflammatory responses caused by some gases. Genetic factors may even regulate the velocity of mucus transport in the trachea (6).

Impairment of clearance mechanisms by inhaled pollutants can significantly affect the retention time of deposited material. Pollutants such as ozone, cigarette smoke, and sulfuric acid alter particle clearance but the direction of this change depends on several factors, including the site of deposition in the respiratory tract (3). Individuals exposed to high concentrations of these agents over long durations may be more susceptible to other agents, particularly those for which residence time in the lung is a key factor in their toxicity.

Selected Agents of Concern

Table 3 presents a number of agents common in indoor air and lists the general sources, health effects, mechanisms, and susceptible populations that have been established for each. While the list of pollutants found in indoor air is exhaustive, the table represents only a partial listing. Most of the agents may be found in both residential and occupational buildings; however, compounds such as nitrogen dioxide and many biological agents are more likely to be present in residential settings.

It should be noted that acute effects associated with the listed agents vary depending on the concentration and duration of exposure. Additionally, a number of other factors may influence an individual's response, including temperature and humidity of the air. Because there is a considerable degree of overlap in the population with regard to thresholds for symptoms and health effects, and because the concentrations of pollutants within residential and occupational buildings vary based on ventilation, specific concentrations of pollutants are not listed.

Cases are indicated where health effects, mechanisms, or susceptible populations were observed only in animals, and not humans. Additionally, cases are noted where results were obtained from elevated concentrations not likely to occur outside of accidental or extreme occupational exposures.

Discussion

Indoor air pollutants range widely from biological agents such as dust mites to chemical irritants such as nitrogen dioxide. Acute adverse health effects associated with these pollutants cover an equally broad spectrum. While the presence of indoor air agents does not necessarily constitute a health risk, a number of factors have contributed to increased concern over and research of indoor air agents. These include tighter building construction, changing lifestyles that have resulted in increased time spent indoors, an expanding knowledge concerning health effects associated with indoor air, and reported increases in indoor-air-related illnesses, including allergic disease (13), airborne infections (14), and multiple chemical sensitivities. Determining mechanisms for specific forms of host sensitivity will be increasingly important as regulatory concerns and scientific interests continue to focus on the indoor air environment.

REFERENCES

1. Samet, J., and M. Utell (1991), "The Environment and the Lung,"Journal of the American Medical Association, 266(5):670-675.

2. Smith, K. (1993), "Taking the True Measure of Air Pollution," EPA Journal, 19(4):6-8

3. Amdur, M., J. Doull, and C. Klaassen (1991), Casarett and Doull's Toxicology, Fourth Edition, Pergamon Press, Inc., Elmsford, N.Y.

4. Terr, Abba I. (1994), "Multiple Chemical Sensitivities," Journal of Allergy and Clinical Immunology, 94:362-366.

5. Lebowitz, M. (1991), "Populations at Risk: Addressing health effects due to complex mixtures with a focus on respiratory effects," Environmental Health Perspectives, 96:35-38.

6. Utell, S. and R. Frank (1989), "Susceptibility to Inhaled Pollutants," American Society for Testing and Materials, ASTM STP 1024.

7. Seltzer, M. (1994), "Building-Related Illnesses," Journal of Allergy and Clinical Immunology, 94(2):351-361.

8. Wanner, H.U. (1993), "Effects of Atmospheric Pollution on Human Health," Experientia, 49:754-758.

9. Menzel, D. (1992), "Antioxidant Vitamins and Prevention of Lung Disease," Annals of the New York Academy of Sciences, 669:141-155.

10. Bardana, E. Jr., and A. Montanaro (1991), "Formaldehyde: An analysis of its respiratory, cutaneous, and immunologic effects," Annals of Allergy, 66:441-452.

11. Chang, C.C., R.A. Ruhl, G.M. Halpern, and M.R. Gershwin (1994), "Building Components Contributors of the Sick Building Syndrome," Journal of Asthma, 31(2):127-137.

12. Bascom, R. (1991), "The Upper Respiratory Tract: Mucous membrane irritation," Environmental Health Perspectives, 95:39-44.

13. Special Article (1993), "Evidence for an Increase in Atopic Disease and Possible Causes," Clinical and Experimental Allergy, 23:484-492.

14. Karol, M. (1991), "Comparison of Clinical and Experimental Data from an Animal Model of Pulmonary Immunologic Sensitivity," Annals of Allergy, 66:485-489.

RELATED ARTICLE: TABLE 2

Explanation of Selected Terms Associated with Both Allergic and Nonallergic Reactions.

Bronchoconstriction. Narrowing of bronchial tubes, providing increased opportunity for inhaled particles to be trapped along the mucous lining of the airway. At least two different mechanisms may be responsible for bronchoconstriction: airway inflammation and activation of irritant nerve receptors and a vagal reflex (3).

Hypersensitivity. State of heightened reactivity to a previously encountered antigen. Mechanisms of hypersensitivity may involve IgE antibody, cellular mechanisms, and others. Additionally, environmental adjuvants have been implicated in hypersensitivity. (Environmental adjuvants are compounds that enhance or potentiate the immune response to a second substance. Concurrent exposure to an environmental adjuvant and a second substance, most often a protein aeroallergen, leads to an immune response mounted toward the second substance.) Airway epithelial injury, altered vagal nerve sensitivity, polymorphonuclear leukocytes, and inflammatory mediators such as arachidonic acid metabolites and tachykinins appear to contribute to airway hyperresponsiveness observed in animal and human studies (5).

Inflammation. Tissue response to injury and invasion by foreign material, characterized by redness, swelling heat, and pain. Inflammation begins as a reaction in the microscopic blood vessels, which enlarge and open their walls allowing cells and mediators to escape from the blood and enter the tissue. Most inflamed tissue contains a mixture of irritative reactions and hypersensitivity responses in their various phases.

Irritation. Irritation is a reflex response of the respiratory system due to stimulation of nerve endings. Activation of the sensory irritant receptor is suspected to occur by two different mechanisms: physical adsorption (believed to be the case for alkanes, alkylbenzenes, alcohols, ketones, and ethers), and chemical reaction (believed to be the case for formaldehyde, acrolein, and chlorobenzylidene malononitriles, and possibly oxidizing agents such as chlorine and ozone) (6). Irritation may also occur as a result of pH extremes and dessication (water removal from tissues) caused by inhaled agents (7).

Corresponding Author: Susan M. Zummo, Staff Scientist, IT Corporation, 2790 Mosside Blvd., Monroeville, PA 15146-2792. Phone: (412)372-7701; Fax: (412)373-7135.
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Author:Karol, Meryl H.
Publication:Journal of Environmental Health
Date:Jan 1, 1996
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