Toxicology arid itidirstrial Health. Vol. 8. No. 3, 1992 213 LETTERS TO THE EDITOR 16 January 1992
Dear Editor: HUMAN EXPOSURE TO BENZO(A)PYRENE: SOME MORE OF THE STORY I read with interest the article by Hattemer-Frey and Travis entitled “Benzo(a)Pyrene: Environmental Partitioning and Human Exposure” in Toxicology and Industrial Health, 7: 141-157, 1991. The article is a thorough academic exercise on how to use literature concentration and dose factor data in making estimates of exposure and dose. As a general indication of which media make the most significant contributions to Benzo(a)pyrene (BaP) exposure the article (model) is correct. Unfortunately, the results demonstrate some of the problems caused by using literature values to describe population exposures, and how a reader can not appreciate the range of error that can be encountered in predictions of exposure without a sensitivity analysis. Our study of BaP exposure/dose (Lioy et al., 1988), was mentioned in the manuscript. It was designed to take actual dietary measurements and other routes of exposure for a population living in Phillipsburg, NJ. The authors state that their estimates of the dose of BaP from food are 70 times higher than our measured values. Since the authors did not have exposure data for the general population or provide a population distribution, the reader cannot determine where our population fits in to the national picture of total exposure to BaP. I do know that our results are consistent since we repeated all measurements within the same population on two other occasions. Our final results were published recently by Waldman et a1 (1991), and as seen in Figure 1 from that article, there is a bimodal distribution for the BaP dose from food consumption. Some people had a low BaP diet and others had a relatively high BaP diet. The conclusion of our total exposure study is the same as the one predicted by the authors: BaP from diet yields the highest exposure. However, for paired samples some individuals received a higher weekly dose from inhalation. This was due to personal lifestyle (e.g.. a person who welded as a hobby). I. am disappointed that the authors did not attempt to complete a sensitivity analysis on their model, and detemiine how they could over estimate exposures in coniparisons to our data. It would have been interesting to match our food questionnaire infomiation to their model inputs. These may have provided some qualitative insights about the differences (Freeman et al., 1991).
Downloaded from tih.sagepub.com at MCGILL UNIVERSITY LIBRARY on March 16, 2015
Recently, our laboratory has taken the question “What is the BaP concentration in prepared foods?” one step further. A project was designed to examine which “cooked foods” contribute to high BaP dietary exposure. Wc conducted a series of controlled experiments on the methods of cooking which increased or decreased the BaP content of food, and included the American favoritehamburger. Frequency
0.3 I
0.1
-
0
25
50
75 100 125 150 175 200 225 250 275 300 ,300
Food BaP (ng/kg)
FIGURE 1. Frequency distribution of BaP concentrations in food samples (from Waldinan et al.. reprinted with permission).
In one set of experiments we measured and compared the BaP content of freshly cooked “fast food” hamburgers purchased from two major national chains. The results showed that the average BaP in “flame-broiled” hamburgers is -a factor of 20 times greater than the average found in the fried hamburgers. These results alone indicate the plausibility of a range in predictions of BaP consumption for hamburgers. Large segments of the population eat “fast food” hamburgers, but they can buy them from one or the other chain (and other sources). This can lead to totally different exposures and doses for this common component to our diet; in fact, a bimodal distribution. The pattern would also hold for other meats prepared using different cooking modalities. Thus, it is not surprising that there can be major “discrepancies” between results when a model is employed that lacks actual population based data. In fact, hamburgers alone niay account for a majority of the difference observed between model predictions and our nieasuremen t s.
Downloaded from tih.sagepub.com at MCGILL UNIVERSITY LIBRARY on March 16, 2015
Tosicology arid liidirstrial Health, Vol. 8, No. 3, 1992
215
The authors’ manuscript does clearly show the need for better and more measurements of exposure to compounds that are of biological significance. If we are to use models for accurate predictions of exposure and risk, they require data from total exposure measurement studies for all pertinent media. Only in this way can we reliably validate a model. Our three-year study in Phillipsburg, NJ, is just an example of types of data that can be used to validate or at least calibrate an exposure model. There is also a major need for population exposure data on specific types of chemicals which can contaminate food during preparation, e.g., BaP, pesticides and lead. Long term dietary exposure data for the general population is just as important as air toxics data. It is a major concern that the authors’ general findings are based on a comparison with studies of the 1970s, and a lack of data to deterniine where our study actually fits within the general population’s exposure to BaP. The U.S. diet and methods of food preparation have changed since the early 1970s. One notable addition is the microwave oven, which produces less BaP in foods. In addition, our diet includes more vegetables. For instance, based on information from the Fresh Fruit and Vegetable Association, cauliflower and broccoli consumption has increased by 300% and 900% (Jaret, 1991). Therefore, estimates of food exposure to BaP and other contaminants need a current baseline before conducting both exposure and risk assessments. Finally, the authors use a mean BaP value (from the 1970s) of 2.5 ng/ni3 in air for their inhalation and deposition estimates. The concentration of BaP has decreased in many areas of the U.S. since the implementation of the 1970 Clean Air Act. A 1982 New Jersey study found the annual average for BaP at 27 locations to be 5 0.8 ng/m3 (7) Phillipsburg had the highest annual average. This city has an iron foundry and pollution control devices were installed to reduce the particulate matter levels. Because of these efforts the most significant source of BAP in our 1987-89 study was residential space heating (Lioy et al., 1988; Waldnian et al., 1991). Recent reports emphasize the need to couple exposure models with measurements (Lioy, 1990; NAS, 1991). Based upon our work, the data required by the authors’ model continues to support this conclusion. REFERENCES
CREIGHTON, P.J., GREENBERG, A., AND LIOY, P.J. (1991). An Investigation of the Effect of Cooking Mcthods on the Benzo(a)Pyrene Concentration of Laboratory-Cooked Meats and of Fast-Food Hamburgers. Presented at the International Conference “Measuring, Understanding, and Predicting Exposures in the 2 1st Century, Atlanta, GA, November 18-21, 1991.
Downloaded from tih.sagepub.com at MCGILL UNIVERSITY LIBRARY on March 16, 2015
2 16
Hattenier-Frey
FREEMAN, N., WALDMAN, J.M., and LIOY, P.J. (1991). Design and Evaluation of a Location and Activity Log Used for Assessing Personal Exposure to Air Pollution. J. Exp. Anal. Environ. Epid. 1: 327-338. HARKOV, R. and GREENBERG, A. (1985). Benzo(a)pyrene in New Jersey. Results from a Twenty-Seven Site Study. JAPCA 35: 234-43. HATTEMER-FREY, H.A. and TRAVIS, C.C. (199 1). Benzo(a)pyrene: Environmental Partitioning and Human Exposure. Tox. Ind. Health 7: 141-157. JARET. P. (1991). Eating your Crucifers Really Can Cut your Changes of Getting Cancer. In Health 5: 59-62. LIOY, P.J. (1990). Assessing Total Human Exposure to Contaminants. .Emiron. Sci. Technol. 24: 938-945. LIOY, P.J., HARKOV, R., WALDMAN, J.M.. PIETARINEN, C.. and GREENBERG, A. (1988). The Total Human Exposure Study (THEES) to Benzo(a)pyrene: Comparison of the Inhalation and Food Pathways. Arch. Environ. Health 43: 304-312. NATIONAL ACADEhW OF SCIENCES (NAS). (1991). Human Exposure Assessment for Air Pollutants. National Academy Press, Washington, DC.pp. 1-321. WALDMAN, J.M.,LIOY, PJ., GREENBERG, A., and BUTLER, J.P. (1991). Analysis of human exposure to benzo(a)pyrene via inhalation and food ingestion in the total human environmental human environmental exposure study (THEES). J. Exp. Anal. Environ. Epid. 1: 193-225. PAUL J. LIOY, PhD Professor and Director, Exposure Measurement and Assessnient Division Environmental and Occupational Health Sciences Institute 681 Frelinghuysen Road, P.O. Box 1179 Piscataway, NJ 08855-1 179
Downloaded from tih.sagepub.com at MCGILL UNIVERSITY LIBRARY on March 16, 2015
Dear Editor: HUMAN EXPOSURE TO BENZO(A)PYRENE: SOME MORE OF THE STORY I read with interest the article by Hattemer-Frey and Travis entitled “Benzo(a)Pyrene: Environmental Partitioning and Human Exposure” in Toxicology and Industrial Health, 7: 141-157, 1991. The article is a thorough academic exercise on how to use literature concentration and dose factor data in making estimates of exposure and dose. As a general indication of which media make the most significant contributions to Benzo(a)pyrene (BaP) exposure the article (model) is correct. Unfortunately, the results demonstrate some of the problems caused by using literature values to describe population exposures, and how a reader can not appreciate the range of error that can be encountered in predictions of exposure without a sensitivity analysis. Our study of BaP exposure/dose (Lioy et al., 1988), was mentioned in the manuscript. It was designed to take actual dietary measurements and other routes of exposure for a population living in Phillipsburg, NJ. The authors state that their estimates of the dose of BaP from food are 70 times higher than our measured values. Since the authors did not have exposure data for the general population or provide a population distribution, the reader cannot determine where our population fits in to the national picture of total exposure to BaP. I do know that our results are consistent since we repeated all measurements within the same population on two other occasions. Our final results were published recently by Waldman et a1 (1991), and as seen in Figure 1 from that article, there is a bimodal distribution for the BaP dose from food consumption. Some people had a low BaP diet and others had a relatively high BaP diet. The conclusion of our total exposure study is the same as the one predicted by the authors: BaP from diet yields the highest exposure. However, for paired samples some individuals received a higher weekly dose from inhalation. This was due to personal lifestyle (e.g.. a person who welded as a hobby). I. am disappointed that the authors did not attempt to complete a sensitivity analysis on their model, and detemiine how they could over estimate exposures in coniparisons to our data. It would have been interesting to match our food questionnaire infomiation to their model inputs. These may have provided some qualitative insights about the differences (Freeman et al., 1991).
Downloaded from tih.sagepub.com at MCGILL UNIVERSITY LIBRARY on March 16, 2015
Recently, our laboratory has taken the question “What is the BaP concentration in prepared foods?” one step further. A project was designed to examine which “cooked foods” contribute to high BaP dietary exposure. Wc conducted a series of controlled experiments on the methods of cooking which increased or decreased the BaP content of food, and included the American favoritehamburger. Frequency
0.3 I
0.1
-
0
25
50
75 100 125 150 175 200 225 250 275 300 ,300
Food BaP (ng/kg)
FIGURE 1. Frequency distribution of BaP concentrations in food samples (from Waldinan et al.. reprinted with permission).
In one set of experiments we measured and compared the BaP content of freshly cooked “fast food” hamburgers purchased from two major national chains. The results showed that the average BaP in “flame-broiled” hamburgers is -a factor of 20 times greater than the average found in the fried hamburgers. These results alone indicate the plausibility of a range in predictions of BaP consumption for hamburgers. Large segments of the population eat “fast food” hamburgers, but they can buy them from one or the other chain (and other sources). This can lead to totally different exposures and doses for this common component to our diet; in fact, a bimodal distribution. The pattern would also hold for other meats prepared using different cooking modalities. Thus, it is not surprising that there can be major “discrepancies” between results when a model is employed that lacks actual population based data. In fact, hamburgers alone niay account for a majority of the difference observed between model predictions and our nieasuremen t s.
Downloaded from tih.sagepub.com at MCGILL UNIVERSITY LIBRARY on March 16, 2015
Tosicology arid liidirstrial Health, Vol. 8, No. 3, 1992
215
The authors’ manuscript does clearly show the need for better and more measurements of exposure to compounds that are of biological significance. If we are to use models for accurate predictions of exposure and risk, they require data from total exposure measurement studies for all pertinent media. Only in this way can we reliably validate a model. Our three-year study in Phillipsburg, NJ, is just an example of types of data that can be used to validate or at least calibrate an exposure model. There is also a major need for population exposure data on specific types of chemicals which can contaminate food during preparation, e.g., BaP, pesticides and lead. Long term dietary exposure data for the general population is just as important as air toxics data. It is a major concern that the authors’ general findings are based on a comparison with studies of the 1970s, and a lack of data to deterniine where our study actually fits within the general population’s exposure to BaP. The U.S. diet and methods of food preparation have changed since the early 1970s. One notable addition is the microwave oven, which produces less BaP in foods. In addition, our diet includes more vegetables. For instance, based on information from the Fresh Fruit and Vegetable Association, cauliflower and broccoli consumption has increased by 300% and 900% (Jaret, 1991). Therefore, estimates of food exposure to BaP and other contaminants need a current baseline before conducting both exposure and risk assessments. Finally, the authors use a mean BaP value (from the 1970s) of 2.5 ng/ni3 in air for their inhalation and deposition estimates. The concentration of BaP has decreased in many areas of the U.S. since the implementation of the 1970 Clean Air Act. A 1982 New Jersey study found the annual average for BaP at 27 locations to be 5 0.8 ng/m3 (7) Phillipsburg had the highest annual average. This city has an iron foundry and pollution control devices were installed to reduce the particulate matter levels. Because of these efforts the most significant source of BAP in our 1987-89 study was residential space heating (Lioy et al., 1988; Waldnian et al., 1991). Recent reports emphasize the need to couple exposure models with measurements (Lioy, 1990; NAS, 1991). Based upon our work, the data required by the authors’ model continues to support this conclusion. REFERENCES
CREIGHTON, P.J., GREENBERG, A., AND LIOY, P.J. (1991). An Investigation of the Effect of Cooking Mcthods on the Benzo(a)Pyrene Concentration of Laboratory-Cooked Meats and of Fast-Food Hamburgers. Presented at the International Conference “Measuring, Understanding, and Predicting Exposures in the 2 1st Century, Atlanta, GA, November 18-21, 1991.
Downloaded from tih.sagepub.com at MCGILL UNIVERSITY LIBRARY on March 16, 2015
2 16
Hattenier-Frey
FREEMAN, N., WALDMAN, J.M., and LIOY, P.J. (1991). Design and Evaluation of a Location and Activity Log Used for Assessing Personal Exposure to Air Pollution. J. Exp. Anal. Environ. Epid. 1: 327-338. HARKOV, R. and GREENBERG, A. (1985). Benzo(a)pyrene in New Jersey. Results from a Twenty-Seven Site Study. JAPCA 35: 234-43. HATTEMER-FREY, H.A. and TRAVIS, C.C. (199 1). Benzo(a)pyrene: Environmental Partitioning and Human Exposure. Tox. Ind. Health 7: 141-157. JARET. P. (1991). Eating your Crucifers Really Can Cut your Changes of Getting Cancer. In Health 5: 59-62. LIOY, P.J. (1990). Assessing Total Human Exposure to Contaminants. .Emiron. Sci. Technol. 24: 938-945. LIOY, P.J., HARKOV, R., WALDMAN, J.M.. PIETARINEN, C.. and GREENBERG, A. (1988). The Total Human Exposure Study (THEES) to Benzo(a)pyrene: Comparison of the Inhalation and Food Pathways. Arch. Environ. Health 43: 304-312. NATIONAL ACADEhW OF SCIENCES (NAS). (1991). Human Exposure Assessment for Air Pollutants. National Academy Press, Washington, DC.pp. 1-321. WALDMAN, J.M.,LIOY, PJ., GREENBERG, A., and BUTLER, J.P. (1991). Analysis of human exposure to benzo(a)pyrene via inhalation and food ingestion in the total human environmental human environmental exposure study (THEES). J. Exp. Anal. Environ. Epid. 1: 193-225. PAUL J. LIOY, PhD Professor and Director, Exposure Measurement and Assessnient Division Environmental and Occupational Health Sciences Institute 681 Frelinghuysen Road, P.O. Box 1179 Piscataway, NJ 08855-1 179
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