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Comments on “Effects of Reducing Lead in Gasoline: An Analysis of the International Experience” SIR: Thomas et al. have recently reported an analysis of temporal trends in the use of lead in gasoline and in population blood lead levels (1). They conclude, in our view mistakenly, that the data point to gasoline lead reductions as the major cause of the reduction in population blood lead levels. Thomas et al. (1) found that for a given location, there is a strong linear correlation between population blood lead and use of lead in gasoline and that as gasoline lead is reduced to zero, blood lead levels across locations converge to a median of 3 µg/dL. From this correlation, Thomas et al. conclude, in our view naively, that gasoline lead reductions have been the main cause of the reduced population blood leads. Unfortunately, their analysis almost wholly ignores the fact that lead reduction strategies have also addressed other sources of lead exposure such as diet and drinking water and that exposure from these pathways has also been substantially reduced. Thomas et al. (1) make passing reference to studies carried out in Christchurch, New Zealand, which reported a nearly 50% drop in blood lead concentrations during a period while gasoline concentrations remained unchanged (2). Hinton et al. (2) attributed the fall in population blood leads to the removal of lead used in soldered food cans and a reduction of canned food consumption. In New Zealand and presumably other developed countries, the removal of lead from food cans took place between 1974 and 1983, a period during which reductions of lead in gasoline were also taking place in many countries. Canned foods represent only one of many sources of lead in the diet, and data from the U.S. FDA show a reduction of dietary lead intake in the United States from 97 µg/day in 1978 to 10 µg/day in 1990 (3). Similar falls in dietary lead exposure are also documented in official data from the United Kingdom (4). While the data from Christchurch, New Zealand, show a reduction in blood lead at a time that petrol lead was almost constant, a government survey from the United Kingdom shows the impact of an abrupt change in lead in gasoline on population blood leads (5). As part of lead reduction policy in the U.K., the mean lead content of gasoline fell from 0.34 g/L in 1985 to 0.14 g/L in 1986. A comprehensive program of blood lead monitoring which took place between 1984 and 1987 shows very clearly, first, that the control populations living in rural areas had blood leads only around 10-20% lower than the exposed urban groups despite very different lead-in-air concentrations (5). Second, for all groups except the traffic police, the decline in blood leads between 1985 and 1986 corresponding to the abrupt change in the lead content in gasoline was of a similar magnitude to that occurring between consecutive years both before and after the lead in gasoline change, when lead in gasoline was relatively constant. The lack of an obvious effect from the reduction in gasoline lead even 2 years after the reduction occurred clearly implies that other sources of exposure were highly influential. Further evidence for the inadequacy of the conclusions drawn by Thomas et al. (1) comes from the calculation of slope factors, which describe the change in blood lead per unit change in lead in air, i.e., ∆PbB/∆PbA. Calculation from the U.S. data in Thomas et al. gives a slope factor of 13.1 ÷ 0.9, which is equal to 14.6 (µg/dL)/(µg/m3). Slope factors 4252
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have been determined both in clinical studies of lead exposure and also in environmental studies and, in the latter case, will take account of indirect pathways of exposure to gasoline lead through, for example, airborne lead deposited into food crops. The U.S. EPA suggests a slope factor of 1.6 (µg/dL)/ (µg/m3) for adults and 1.9 (µg/dL)/(µg/m3) for children in its Air Quality Criteria for Lead report (6). An independent review suggests values of 3-5 (µg/dL)/(µg/m3) for children (7). Clearly, slope factors determined from a simplistic assumption that changes in population blood lead over a period of several years result solely from changes in air lead from lead in gasoline yield quite unrealistic values because of the decline in other sources of exposure. Lead in drinking water in areas of high plumbosolvency has been a major cause of elevated population blood lead concentrations. Watt et al. (8) reported that 17% of Glasgow households had water lead concentrations of 10 µg/L or more in 1993 as compared with 49% of households in 1981 because of a vigorous program of control measures. Even in 1993, however, tap water lead remained the main correlate of raised maternal blood lead concentrations and accounted for 62% and 76% of cases of maternal blood lead concentrations above 5 and 10 µg/dL respectively (8). There have been very many other published studies relating drinking water lead exposure to population blood leads showing a clear impact of this pathway of exposure (e.g., refs 9-11). Lead in paint and lead in dusts and soils can be an important exposure pathway for some individuals, particularly for children. In general, remedial action has led to a reduction in these exposure pathways also, although the data show a less clear link to blood leads except in individual cases of exceptionally high exposure. While the use of lead in gasoline has undoubtedly contributed to the lead content of soils and dusts, other factors such as leaded paint and the age of the house play a major role in determining lead concentrations in soils and dusts (12, 13). Reductions in lead in gasoline will not bring about rapid changes in the lead content of these media, especially housedust. Another issue that needs to be addressed is that of the common intercept in the trends of blood lead versus gasoline lead of around 3.0 µg/dL. This is likely to be the result of comparable policies being introduced in countries that have implemented a lead control strategy, which have impacted in a broadly similar way on the lead content of food and of drinking water, exposure media whose lead content is affected rather little by the use of lead in gasoline. Clearly, lead exposures from these media have been reduced to similar levels in the various countries, which is hardly surprising given the internationalization of both science and trade. Clearly, there is overwhelming evidence that not only do sources other than gasoline lead contribute to population blood leads but also that such exposures have been declining in developed countries over the same time period as reductions in lead in gasoline have taken place. For countries embarking on a lead control program, it is very important that they recognize that lead is a multi-media pollutant and that attention to all sources of exposure is a prerequisite to effective reduction in population blood leads.
Literature Cited (1) Thomas, V. M.; Socolow, R. H.; Fanelli, J. J.; Spiro, T. G. Environ. Sci. Technol. 1999, 33 (22), 3942-3948. (2) Hinton, D.; Coope, P. A.; et al. J. Epidemiol. Commun. Health 1986, 40, 244-248. (3) Bolger, P. M.; Yess, N. J.; Gunderson, E. L.; Troxwell, T. C.; Carrington, C. D. Food Addit. Contam. 1996, 13, 53-60. 10.1021/es991425s CCC: $19.00
2000 American Chemical Society Published on Web 09/01/2000
(4) U.K. Ministry of Agriculture Fisheries and Food. Lead in Food: Progress Report; Twenty Seventh Report; HMSO: London, 1989. (5) U.K. Department of the Environment. U.K. Blood Lead Monitoring Programme 1984-1987. Pollution Report 28; HMSO: London, 1990. (6) U.S. Environmental Protection Agency. Air Quality Criteria for Lead; EPA/600/8-83/028Af; EPA: Research Triangle, NC, 1986.
(11) Sherlock, J. C.; Ashby, D.; Delves, H. T.; Forbes, G. I. Human Toxicol. 1984, 3, 383-392. (12) Culbard, E. B.; Thornton, I.; Watt, J.; Wheatley, M.; Moorcroft, S.; Thompson, M., J. Environ. Qual. 1988, 17, 226-234. (13) Thornton, I.; Davies, D. J. A.; Watt, J. M.; Quinn, M. J. Environ. Health Perspect. 1990, 89, 55-60.
(7) Brunekreef, B. Sci. Total Environ. 1984, 38, 79-123.
Roy M. Harrison* and Martin Whelan
(8) Watt, G.; Gilmour, W.; Moore, M.; Murray G.; Womersley, J. Br. Med. J. 1996, 313, 979-981.
Division of Environmental Health and Risk Management The University of Birmingham Edgbaston Birmingham B15 2TT, United Kingdom
(9) Elwood, P. C.; Gallacher, J. E. J.; Phillips, K. M.; Davies, B. E.; Toothill, C. Nature 1984, 310, 138-140. (10) Pocock, S. J.; Shaper, A. G.; et al. J. Epidemiol. Commun. Health 1983, 37, 1-7.
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