Direct and indirect exposure to air pollution

Direct and indirect exposure to air pollution

Direct and indirect exposure to air pollution RAYMOND W. THRON, PhD,Minneapolis, Minnesota Hazardous substances that originally are discharged as air ...

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Direct and indirect exposure to air pollution RAYMOND W. THRON, PhD,Minneapolis, Minnesota Hazardous substances that originally are discharged as air pollutants may find their pathway to human exposure through multiple routes, including ingestion and dermal contact, as well as direct inhalation. The mechanisms for modeling and understanding the fate of air pollutants through atmospheric transport, deposition into water and soil, bioaccumulation, and ultimate uptake to receptor organs and systems in the human body are complex. Pollution prevention programs can be better engineered, pollution priorities can be identified, and greater environmental public health gains [attributable to pollution prevention] can be achieved by evaluating the multiple pathways to human exposure and through improved dosage calculations. A single contaminant source often may represent only a fraction of a total body pollutant burden. Further research is needed on source culpability and attributable risk, long-range transport of air pollutants, human dose contributions by various pathways, better techniques for health risk assessment, and an identification of human behavior patterns that affect exposure and dose. [OTOLARYNGOLHEAD NECK SURG 1996; 1t 4:281-5.]

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[=ully effective pollution prevention activities require an examination of the multiple pathways of exposure for the contaminants under consideration. Pollution prevention activities include reduction or elimination of the contaminants at the source and reduction of the contaminants through some type of processing or intervention and through avoidance of human exposure. Avoidance of human exposure, although not strictly a pollution prevention activity, is often needed when immediate actions are required or when pollution control costs are high. The number of "nonattainment" air quality areas in the United States has steadily declined. Currently there are 43 nonattainment areas for ozone and 10 for carbon monoxide in the United States compared with 98 and 43 areas, respectively, in 1990. The number of nonattainment areas for other criteria pollutants have similarly declined. For nitrogen oxides, there were no nonattainment areas. These statistics, as released by the U.S. Environmental Protection Agency (USEPA), provide an overall

From the Freshwater Foundation. Presented at the conference "Air Pollution Impacts on Body Organs and Systems"of the National Associationof Physicians for the Environment, the National Press Club, Washington, D.C., Nov. 18, 1994. Received for publication July 6, 1995;revisionreceived Sept. 29, 1995; accepted Sept. 29, 1995. Reprint requests: RaymondW. Thron, PhD, 2701 S. E. University Ave., Suite 203, Minneapolis, MN 55414-3236. Copyright © 1996by the American Academyof OtolaryngologyHead and Neck Surgery Foundation, Inc. 0194-5998/96/$5.00 + 0 23/1/69441

indication of trends. 1Comparable information, however, is lacking regarding the "hazardous" and other "noncriteria" air pollutants. Information available from the toxics release inventory, compiled annually by states and the USEPA, provides some data, but this information does not adequately incoroprate the human exposure variable. Expensive pollution control activities may make little sense if the attributable risk to the exposure is small or insignificant. The challenge lies in the work necessary to identify how the total exposure risk is attributed to various contaminant sources and multiple pathways of exposure. Air pollution remains an important risk to public health, despite the many improvements that have been made in outdoor ambient air qualityY As part of the national health objectives for the year 2000, one objective is to reduce exposure to air pollutants so that at least 85% of persons live in counties that meet the U S E P A standards. Even by the year 2000, many people will remain exposed to exceedance levels for those air pollutants for which standards exist. This goal and these statistical objectives do not, however, take into account other multiple source exposures, many of which may be from indoor exposures and exposure through water and food. With the initial passage of the Clean Air Act, pollution prevention activities were virtually 100% dominated with ambient outdoor air quality: Since the mid-1980s an increased emphasis has been placed on indoor air exposures. This is in recognition of the majority time that is spent indoors and of the 28t

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Table I. Prevalence of blood lead levels in children 1 to 5 years of age Blood lead level [l~g/dl)

NHANES II [%)

NHANES III (%]

-->10 ->15 ->25

88.2 53.0 9.3

8,9 2.7 0,5

Confidence interval is 90%; blood lead level expressed a s geometric mean.

deteriorating indoor air quality caused by energy efficiency programs and indoor air emissions from building materials and products. The Occupational Safety and Health Administration (OSHA), in recognition of potential indoor air hazards at the nonindustrial workplace, has proposed the establishment of indoor air standards. The basis for this proposed action is a preliminary determination that employees working indoors face a risk of health impairment because of poor indoor air quality. The provisions of the proposed OSHA standard would apply to all indoor "nonindustrial work environments." Additionally, all work sites, both industrial and nonindustrial within OSHA's jurisdiction, would be covered against provisions addressing environmental tobacco smoke. Employers would be required to implement controls for specific contaminants and their sources, such as outdoor air contaminants, microbial contamination, maintenance and cleaning chemicals, pesticides, and other hazardous chemicals within indoor work environments. MASS BALANCE APPROACH

Traditional pollution control activities have focused on point sources of pollution. Typically, emission limitations are set by regulatory bodies through mechanisms only partially related to actual human exposure. Human exposure to air pollutants is an extremely complex scenario that is difficult to accurately model. The total exposure assessment methodology (TEAM) study began, in part, to approach this problem through research on individual exposures during an individual's daily activities at work and home. 4 The study was looking at a total body burden for selected contaminants. To correctly portray and quantify human exposure, a mass balance evaluation of the air contaminant under consideration should be done. 5 The factors involved in doing a mass balance evaluation include a determination of the fate, transport, and ultimate uptake to receptor organs and systems in the human body. The task is neither easy nor simple

because of the numerous variables, which themselves are dependent on the pollutant agent. The development of models to predict how toxic air pollutants may affect large ecosystems like the Great Lakes or microsystems like your home will require continuing major advances in our state of knowledge. Information and knowledge will need to be developed on identifying populations and communities affected, identifying the appropriate end points in the response to human exposure, and better understanding the numerous environmental variables (including community characteristics) that influence the response. The problem of many contaminants being cumulative and persistent makes model development difficult. The issue of multiple chemical sensitivities by some individuals can also make the determination of health effect threshold levels difficult to compute. INDIRECT EXPOSURES TO AIR TOXICS: EXAMPLES Mercury, Polychlorinated Biphenyls, and Dioxin

Numerous examples exist of air toxics whose fate and transport result in indirect human exposure. Human exposure to mercury, polychlorinated biphenyls (PCBs), and dioxin can result from eating sport or commercially caught fish. 6 These contaminants may have come from an air pollution source or through a discharge to a water body. Air deposition of these contaminants onto water and subsequent settling in sediments results in a bioaccumulation of these contaminants in f i s h . 7'8 People who eat fish are subsequently exposed to varying doses of these contaminants. Often these contaminants are not detected in water, but only in the fish taken from the rivers and lakes. Actual human exposure will vary according to the amount of actual contaminants in the fish, frequency of eating the fish, and the size, type, and manner of preparing the fish. Removing the skin of fish and trimming the fillets can reduce PCBs and dioxin exposure by 20% to 50%. This occurs because PCBs and dioxin concentrate in the fatty tissues of fish.

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Broiling, baking, or grilling fish so that the fat drips away will further reduce exposure. Mercury, to the contrary, tightly binds to proteins in all fish tissue and will not be reduced by the above preparation techniques. Also, the type of fish eaten will affect exposure. Mercury and PCBs build up in predator fish, whereas their prey, such as perch, bluegill, sunfish, and crappie, have fewer contaminants. Mercury, as an example, recycles through land, water, and air and can enter both plant and animal tissue. Mercury is a naturally occurring metal; however, most mercury found in water comes from the air. Once in water, the mercury is converted to methylmercury by bacteria and other processes. Major sources of mercury air emissions are from the household and industrial incineration of waste and latex paints and from the burning coal and other fossil fuels. Mercury levels in many waters are gradually decreasing because of stringent mercury-emission limitations imposed on the operation of incinerators and utilities. The human exposure to these contaminants, through eating fish, can be the result of air emissions hundreds or thousands of miles away. The short- and long-range transport of these pollutants is difficult and complex to accurately model. PCBs in water are traceable back to their original uses in electrical transformers, cutting oils, and carbonless paper. PCBs were banned in 1976; however, they do not easily decompose and will remain in lakes and rivers for years. Although levels are declining, it may be another 20 years before the PCB levels are insignificant. Dioxin is typically an unwanted by-product of incineration and some industrial processes that use chlorine. Although air pollution is the predominant original transport route, human exposure has resulted from inhalation, ingestion, and contact. Lead

Lead is an excellent example of potential human exposure through multiple pathways. This naturally occurring element has been in use since the early beginnings of our civilization. Lead is ubiquitous in our environment; virtually no one is without some exposure. Reducing lead exposure among infants, toddlers, and preschool children is particularly important because the developing nervous system is sensitive to lead toxicity.9-~2Although there has been a very dramatic decline in lead exposure among children, nearly 1.7 million children aged 1 to 5 years have blood lead levels equal to or greater than 10 p.g/dl. Cognitive development may be affected at levels above 10 p.g/dl. 13'14

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Major sources of lead exposure have come from the use of lead in paint, gasoline, water distribution systems, food, hobby activities, and various substance use. 15Lead exposure attributable to air emissions from automobiles was a major exposure source before 1976. Between 1976 and 1990, lead used in gasoline declined by 99.8%. Additionally, the use of lead in food and soft drink cans manufactured in the United States declined to less than 1% in 1990.16The decline in the prevalence of blood lead levels in children 1 to 5 years of age, as observed from data in the National Health and Nutrition Examination Study (NHANES) II and III, is shown in Table 1. Data (Table 2) from phase I of the NHANES III study show that infants, toddlers, and preschool children remain at greatest risk. In the 20- to 74-year age group the blood lead level gradually increased beginning at 1.6 Ixg/dl.17'1s In the United States, the major sources of lead exposure culpability have shifted to paint and water distribution systems and fixtures. To the contrary, in eastern Europe and many developing countries, the air contribution to lead exposure remains high. 19 Even bulk-delivered water has been found with high lead concentrations because lead has leached from lead-soldered seams and brass fittings, particularly in older storage tanks. Lead in soil around homes remains a potential problem because of the previously deposited air lead and deteriorating house paint. 2022 Exposure and uptake of lead into the bloodstream is not universally consistent. It will, among other things, depend on individual behavior patterns, parental supervision, and diet. Radon

Radon provides an example of two principal pathways for exposure: inhalation and ingestion. Human radon exposure can occur through inhalation of the radon gas as it enters the home from external soil and rock through small basement openings in the foundation and flooring. Additional radon may be added to the indoor air through the transfer of radon in drinking water to air at the rate of approximately 1 pCi/L for every 10,000 pCi/L of radon in water, although some studies indicate that this ratio may be greater by a factor of 2 to 5. 8 In indoor air the decay of radon is influenced by the ventilation rate in the home. Indoor air movements and how they influence the human dose rate have to be uniquely determined. Ingestion of water containing radon may contribute to the total body burden. Although data are limited, some models establish the risk from the

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T a b l e 2. NHANES III b l o o d l e a d levels (1988-1991) Population group

Blood lead level [ixg/dl)

U.S, population 1-2 years 12-19 years 20-74 years

2.8 4,1 1.6 > 1.6

Confidence interval is 95%; blood lead level expressed as geometric mean.

ingestion pathway for waterborne radon from 25% to 100% of the risk from inhalation.8 The decay of radon from water that is ingested is affected by biologic processes, including radon exchange rates from the stomach to the lung. Water that is ingested without heating or agitation retains approximately 80% to 90% of the original concentration of radon in the water. After ingestion, the radon is transported throughout the gastrointestinal tract and ultimately into the bloodstream. In the bloodstream the ingested radon can move to various organs and tissues of the body, where subsequent decay leads to the emission of primarily a-radiation. 23 Considerable additional work is needed to better understand radiation exposure from radon-rich water. Current research continues to support the conclusions that inhalation of radon and radon progeny are the primary pathways of concern. C O N C L U S I O N A N D RESEARCH A G E N D A

An accurate assessment of human exposure and dose to hazardous agents and a better understanding of the toxicity and biologic fate, transport, and human uptake of the hazardous agents are needed. 24 With a better understanding of these issues, pollution prevention programs can be better engineered and implemented, and a rationale for emission limitations can be better justified. Continued research is necessary to better comprehend the full effects of air pollution, recognizing that human exposure to air contaminants through inhalation is only a fraction of the total exposure for the same hazardous agent. Some research agenda issues include the following. 1. A better determination of source culpability and attributable risk. 2. Improved understanding of the short- and long-range transport of air pollutants, including chemical transformations and breakdown products that may result during transport. 3. A better modeling of the mechanisms of actual dose to human beings, particularly as to their effects on different body organs and systems.

Closely paralleling this issue is the delineation and human dose contributions by various exposure pathways, that is, inhalation, ingestion, and dermal contact. 4. Improved techniques for health risk assessment. 5. An identification of human behavior patterns that affect exposure and dose. REFERENCES

1. Curran T, Faoro R, Fitz-Simons T, et al. National air quality and emissions trends report. Research Triangle Park, N.C.: US Environmental Protection Agency, Office of Air Quality Planning and Standards, October 1993; publication no. EPA454/R-93/031. 2. Dockery DW, Pope CA. Acute respiratory effects of particulate air pollution. Annu Rev Public Health 1994;15:107-32. 3. Schwartz J. Air pollution and daily mortality: a review and meta analysis. Environ Res 1994;64:36-52. 4. Calabrese EJ, Kenyon EM. Air toxics and risk assessment. Chelsea, Mich.: Lewis Publishers, Inc., 1991. 5. Hallenbeck WH. Quantitative risk assessment for environmental and occupational health. Chelsea, Mich.: Lewis Publishers, Inc., 1993. 6. Flint RW, Vena J. Human health risks from chemical exposure: the Great Lakes ecosystem. Chelsea, Mich.: Lewis Publishers, Inc., 1991. 7. Mehlman MA, ed. Health hazards and risks from exposure to complex mixtures and air toxic chemicals. Princeton, N.J.: Princeton Scientific Publishing Co., Inc., 1991. 8. Wang RGM, ed. Water contamination and health: integration of exposure assessment, toxicology, and risk assessment. New York, N.Y.: Dekker, 1994. 9. Weitzman M, Glotzer D. Lead poisoning. Pediatr Rev 1992; 13:461-8. 10. Bellinger D, Sloman J, Leviton A, Rabinowitz M, Needleman HL, Waternaux C. Low-level lead exposure and children's cognitive function in the preschool years. Pediatrics 1991;87: 219-27. 11. Hayes DB, McElvaine MD, Orbach HG, Fernandez AM, Lyne S, Matte TD. Long-term trends in blood lead levels among children in Chicago: relationship to air lead levels. Pediatrics 1994;93:195-200. 12. Holly AR, Bijur PE, Markowitz M, Ma Y, Rosen JF. Declining blood lead levels and cognitive changes in moderately lead-poisoned children. JAMA 1993;269:1641-6. 13. Centers for Disease Control and Prevention. State activities for prevention of lead poisoning among children-United States, 1992. MMWR 1993;42:171- 2. 14. Needleman HL, Gatsonis CA. Low-level lead exposure and the IQ of children. JAMA 1990;263:673-8, 15. Agency for Toxic Substances and Disease Registry. The nature and extent of lead poisoning in children in the United States: a report to Congress. Atlanta, Ga.: U.S. Department of Health and Human Services, 1988. 16. Centers for Disease Control and Prevention. Blood lead levels-United States, 1988-1991. MMWR 1994;43:525-6. 17. Brody DJ, Pirkle JL, Kramer RA, et al. Blood lead levels in the U.S. population from phase 1 of the Third National Health and Nutrition Examination Surveys. JAMA 1994;272: 277283. 18. Pirkle JL, Brody DJ, Gunter EW, et al. The decline in blood

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lead levels in the United States: the National Health and Nutrition Examination Surveys. JAMA 1994;272:284-91. 19. Jedrychowski W. Total human exposure to lead among the general population in Poland. Public Health Rev 1992;19: 135-40. 20. Centers for Disease Control and Prevention. State activities for prevention of lead poisoning among c h i l d r e n - U n i t e d States, 1992. MMWR 1993;42:171-2. 21. Strategy for reducing lead exposures. Washington, D.C.: U.S. Environmental Protection Agency, 1992.

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22. Weitzman M, Aschengrau A, Bellinger D, Jones R, Hamlin JS, Beiser A. Lead-contaminated soil abatement and urban children's blood lead levels. JAMA 1993;269:1647-54. 23. Jayanty RKM, Peterson MR, Naugle DF, Berry MA. Exposure assessment: methods of analysis for environmental carcinogens. Risk Anal 1990;10:587-96. 24. U.S. Congress, Office of Technology Assessment. Researching health risks. Washington, D.C,: U.S. Government Printing Office, 1993.