Air Pollution from Traffic at the Residence of Children with Cancer
Ole Raaschou-Nielsen1,
Ole Hertel2,
Birthe L. Thomsen1 and
Jørgen H. Olsen1
1 Danish Cancer Society, Institute of Cancer Epidemiology, Copenhagen, Denmark.
2 National Environmental Research Institute, Roskilde, Denmark.
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ABSTRACT
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The hypothesis that exposure to traffic-related air pollution increases the risk of developing cancer during childhood was investigated. The authors enrolled 1,989 children reported to the Danish Cancer Registry with a diagnosis of leukemia, tumor of the central nervous system, or malignant lymphoma during 19681991 and 5,506 control children selected at random from the entire childhood population. The residential histories of the children were traced from 9 months before birth until the time of diagnosis of the cases and a similar period for the controls. For each of the 18,440 identified addresses, information on traffic and the configuration of streets and buildings was collected. Average concentrations of benzene and nitrogen dioxide (indicators of traffic-related air pollution) were calculated for the relevant period, and exposures to air pollution during pregnancy and during childhood were calculated separately. The risks of leukemia, central nervous system tumors, and all selected cancers combined were not linked to exposure to benzene or nitrogen dioxide during either period. The risk of lymphomas increased by 25% (p for trend = 0.06) and 51% (p for trend = 0.05) for a doubling of the concentration of benzene and nitrogen dioxide, respectively, during the pregnancy. The association was restricted to Hodgkin's disease.
air pollution; benzene; child; Hodgkin disease; neoplasms; nitrogen dioxide
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INTRODUCTION
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In many countries, road traffic is the major source of ambient air pollution in urban areas, where most people live. Air pollution from traffic is a complex mixture of many chemicals, of which several are known or suspected carcinogens (1
). The evidence for the carcinogenicity of traffic exhaust derives mainly from experiments in animals and studies of occupationally exposed persons. In 1989, however, a case-control study performed in Denver, Colorado, showed elevated risks of cancer among children living near streets with high traffic density (2
), and two studies from Sweden (3
) and the United Kingdom (4
) indicated an elevated risk of cancer among children living at addresses with high levels of ambient air pollution. These results have raised great public concern. The shortcomings of these three studies include limited sample sizes and crude methods for assessing exposure based on only part of the residential history of the children. Large studies with improved methods are required to address the hypothesis and the public concern properly.
The present study was designed as a case-control study to test the hypothesis that air pollution from traffic causes cancer in childhood. The level and extent of past exposure to exhaust fumes at the residences of children with the most common types of cancer were evaluated and compared with those of a population-based, random sample of children without cancer. The exposure assessment method was validated against measurements of air pollution.
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MATERIALS AND METHODS
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Study population
The cases of cancer in this study were those of children born after December 31, 1959, who received a diagnosis of leukemia, tumor of the central nervous system, or malignant lymphoma when they were under the age of 15 years, during the period from January 1, 1968, to December 31, 1991. They were identified from the files of the Danish Cancer Registry, which also provided the name and personal identification number. This number, which is unique to every Danish citizen, incorporates sex and date of birth and permits accurate linkage of information among registers. The nationwide cancer registration system, set up in 1942, has been described and evaluated previously (5
). The register also includes histologically benign tumors of the brain and intracranial meninges. Children born outside Denmark were excluded, leaving a total of 1,989 children with cancer for the study (table 1).
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TABLE 1. Cases of childhood cancer diagnosed in Denmark during 19681991 among children born in 1960 or later and matched controls
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Control children were drawn from the files of the Danish Central Population Registry and likewise identified by name and personal identification number. They had to have been born in Denmark and, at the time of the diagnosis of the corresponding case, to have been alive without a diagnosis of cancer and residing in Denmark. Two, three, and five controls matched by sex, age (exact), and calendar time (within 1 year) were chosen for each case of leukemia, central nervous system tumor, and malignant lymphoma, respectively, for a total of 5,506 children included as controls (table 1).
Residential history
Information on the parents of case children and control children and on the number of the index child in the sibship (birth order) was obtained from the files of the Central Population Registry. The residential histories of each family were ascertained retrospectively from the date of diagnosis of cancer or a similar date for the matched control children (referred to in the following as "date of diagnosis") to 9 months before the child's birth. Addresses were provided jointly by the Central Population Registry and the 275 local population registries of Denmark. Each location was identified according to county, municipality, town, postal code, street, building number, floor, and side; the dates of moving in and leaving the address were noted. The families were not approached directly. Altogether, we identified 18,440 addresses at which the 7,495 pregnant mothers and children had lived. The residential history was incomplete for 301 families (4 percent); no information at all was available for 98 mothers during the pregnancy (20 cases, 78 controls) and for nine children during childhood (one case, eight controls).
Exposure assessment
Benzene and nitrogen dioxide (NO2) are commonly used markers of traffic-related air pollution and were used as such in this study. The average concentrations of benzene and NO2 at the front door of each dwelling during the period that the families occupied the address were acssessed by use of a modified version of the Operational Street Pollution Model (6




12
). Briefly, the model can be used to calculate air pollution levels from information on the exact configuration of the street in front of the address (the width of the street, the height of the buildings and their distance from the street, and street sections with no buildings), the traffic density on the street (vehicles per day), the proportion of vehicles weighing more than 3,500 kg, the average traffic speed (km/h), and the presence of other streets within 50 m with a traffic density higher than that on the index street, in combination with information on emission factors (g/km) for the Danish car fleet, meteorologic variables (wind speed, temperature, and solar radiation), and background levels of air pollution.
The data on the street configuration, the traffic pattern, and the degree of urban development for each of the 18,440 addresses occupied by the 7,495 study subjects were collected for the relevant period by use of a registration scheme designed for this purpose (12
). Staff from each of the 275 municipal highway departments of Denmark filled in a registration form for each address in their municipality, without knowledge of the case or control status of the children. All of the 18,440 schemes were filled in and returned. Meteorologic data, obtained from Copenhagen Airport, were considered to be representative of Denmark as a whole. The geographic distribution and temporal variation in background air pollution levels were estimated from measurements made during 19941995 at four sites in different parts of Denmark and from information on changes in air pollution emissions in Denmark since 1960 (13
).
Potential confounding factors
The degree of urban development was calculated as the average category of all residences of the child, weighted by the length of each residential period. The categories were as follows: 1, rural area; 2, <2,000; 3, 2,00019,999; 4, 20,00039,999; 5, 40,00079,999; 6, 80,000149,999; and 7,
150,000 inhabitants in the town. The type of residence was scored according to the proportion of time the child had lived in a one-family house (villa, row house, farmhouse, etc.) or an apartment. The address at birth was used to allocate each child to one of eight geographic regions of Denmark. Trained employees of the Danish electric utility companies investigated each address for proximity to 50- to 400-kV overhead lines, underground cables, or transformer stations during the relevant residential period, and the average electromagnetic field strength at the address was calculated (14
). Moreover, we considered the mother's age and the birth order of the child as potential confounding factors. The degree of urban development and the type of residence were considered for the pregnancy and the childhood period separately, whereas exposure to an electromagnetic field was assessed for the two periods combined.
Statistical analyses
The risk of childhood cancer was analyzed according to the traffic density and air pollution level at the residence during the pregnancy and during childhood. Exposure of the mothers to benzene and NO2 was summarized as "exposure level x time" for each address occupied from the presumed date of conception until the date of birth of the child. The residential history of 98 mothers was unknown for the entire pregnancy, leaving 7,397 children (99 percent) available for these analyses.
Cumulated exposure during childhood was calculated from the date of birth until 12 months before the date of diagnosis, with an additional requirement of at least 6 months of follow-up of the exposure of the child. Thus, 697 children (cases and matched controls) in whom cancer had been diagnosed before they reached 18 months of age were not included in the analyses of childhood exposure, and no information on exposure was available for nine of the remaining children, leaving 6,789 children (91 percent) available for these analyses. The time period for which exposure was calculated was exactly equal for a case and the matched controls.
If a pregnant mother or a child had lived at an unidentified address during part of the relevant period, that address was assigned the exposure level that corresponded to the time-weighted average at the known addresses.
Because of the nested case-control design of the study, with equal follow-up time for a case and the matched controls, the rate ratios (15
) (henceforth denoted relative risks) for childhood cancer were estimated by conditional logistic regression analysis with the "Phreg" procedure of SAS (16
). Four categories of exposure to air pollution were defined, with the 50th, 90th, and 99th percentiles as cutoff points. Exposure was log-transformed in the trend analyses, such that an excessive influence of a few extremely high values was avoided, and a doubling of the exposure corresponded to a fixed relative risk independently of the exposure level. Trend tests for residential traffic density were done similarly.
Validation of exposure assessment
We estimated how many of the children allocated to each category of exposure could be expected to have been correctly classified. In a separate validation study, we included 204 children living in Copenhagen or in rural areas outside Copenhagen and measured the NO2 concentration outside the front door of each dwelling during 6 months (11
) and the personal exposure to NO2 of each child during 1 week (17
). Following exactly the same procedures as in the case-control study, we collected information about streets, buildings, and traffic and calculated the concentrations of NO2 at each residence. Thus, the validation study provided information about the relation between 1) the calculated and measured half-year average concentration of NO2 at the front door and 2) the calculated 1-week average concentration of NO2 at the front door and simultaneously measured personal exposure.
For every calculated average concentration of NO2 at the front door in the case-control study during the pregnancy, we estimated the probability of falling into different categories of measured concentrations; that is, we fitted a linear relation, with a slope fixed at 1, between the log-transformed calculated and measured concentrations of NO2 and used this line and the estimated standard deviation around the line to predict the probability. The probabilities for each individual were accumulated into expected numbers of children within each category, thus providing the expected number of misclassified children in each category of exposure in the case-control study. Cutoff points among the different categories of measured exposure were defined to obtain the same expected numbers of children in each category as in the corresponding category of the case-control study. The statistical method for estimating the distribution of the measured concentrations has been described by Secher et al. (18
). The same procedure was used for personal exposures, except that the relation between personal exposure and the calculated front-door concentration was estimated by standard linear regression.
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RESULTS
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Cases and controls were similar with regard to the mother's age, birth order, residential region at the time of birth, degree of urban development, the proportion of time they had lived in a one-family house, and exposure to an electromagnetic field, although a slightly smaller proportion of case than control children was born in the Copenhagen area and a slightly larger proportion of case children had lived in a one-family house (table 2).
Traffic density
No increased risk of leukemia, central nervous system tumors, lymphomas, or these diagnoses combined (denoted "all cancers") was associated with exposure to high traffic density during pregnancy or childhood in comparison with exposure to less than 500 vehicles per day, even when the density was more than 10,000 vehicles per day at the residence. The trend analyses showed no significant results (table 3).
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TABLE 3. Crude relative risks (RRs) and 95% confidence intervals (CIs) for childhood cancers associated with residential traffic density, Denmark, 19681991
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Air pollution
The predicted exposures to the two different indicators of traffic-related air pollution were correlated; the correlation coefficient (Pearson's) was 0.71 for the pregnancy (n = 7,379) and 0.83 for the childhood period (n = 6,789).
The results showed no increased risk of developing "all cancers" in association with the three higher categories of exposure when the lowest category was used as reference (table 4). No effect was seen even in the highest categories of exposure to both pollutants, and this result was the same for both exposure periods. The trend analyses indicated no effect of air pollution on the risk of "all cancers." The unadjusted (crude) and adjusted relative risks differed very little. Similarly, the risks of developing the two major types of childhood cancer, leukemias and central nervous system tumors, were not increased at the higher categories of exposure, and no significant trends were found, no matter which pollutant or exposure period was considered. Actually, a weak, nonsignificant tendency for an inverse association between exposure and the risk of these two types of cancer was seen in most cases.
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TABLE 4. Crude and adjusted* relative risks (RRs) and 95% confidence intervals (CIs) for childhood cancers associated with air pollution at the residence, Denmark, 19681991
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The results indicated an association between exposure in utero and the risk of developing lymphomas (table 4): The relative risks increased with increasing category of exposure to both pollutants. The exception was the highest category of exposure to benzene; however, the confidence interval was wide for this relative risk estimate. The exposure-response pattern was confirmed in the trend analyses, which showed a 25 percent (p for trend = 0.06) and a 51 percent (p for trend = 0.05) increase in risk of doubling the concentrations of benzene and NO2, respectively. The association between the risk of lymphomas and exposure during childhood was less consistent. The highest category of exposure to benzene was associated with a decreased risk, but the opposite was observed for exposure to NO2. Correspondingly, the trend estimates indicated effects in opposite directions for the two markers of traffic-related air pollution but were not significantly different from the neutral value (both p for trend > 0.80) (table 4).
Analyses by morphologic subtype showed that the increased risk of lymphomas in association with exposure to benzene and NO2 in utero was restricted to Hodgkin's disease. In the adjusted analyses, the highest categories of exposure to benzene and NO2 resulted in 4.3 and 6.7 times higher risks of Hodgkin's disease than the reference category (table 5). The trend analyses showed an 84 percent (p for trend = 0.005) and a 147 percent (p for trend = 0.02) increase in risk of doubling the concentrations of benzene and NO2, respectively. Separate analyses for children below and above the median age at diagnosis (11.7 years) showed that the association was restricted to children who received their diagnosis at younger ages (p for trend = 0.001 for benzene and 0.009 for NO2; data not shown). Unadjusted analyses showed weaker associations of only borderline significance; the difference between the crude and adjusted risk estimates (table 5) was caused primarily by adjustment for degree of urban development. There was no significant relation between the risk of Hodgkin's disease and exposure during childhood. Moreover, the results showed no significantly increased risk of non-Hodgkin's lymphoma or any of the morphologic subtypes of leukemia (acute lymphocytic leukemia, acute nonlymphocytic leukemia) or of central nervous system tumors (ependymoma, astrocytoma, medulloblastoma) in association with exposure to benzene or NO2 during any of the exposure periods (data not shown). An analysis restricted to children in whom acute lymphocytic leukemia was diagnosed when they were below age 5 (the childhood peak) and the matched control children showed no increase in risk in association with exposure to air pollution.
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TABLE 5. Crude and adjusted* relative risks (RRs) and 95% confidence intervals (CIs) for Hodgkin's disease associated with air pollution at the residence during pregnancy, Denmark, 19681991
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All of the analyses of the associations with air pollution were repeated after exclusion of children whose residential history was not fully identified. This had only minor effects on the results.
Validation of exposure assessment
Figure 1 (top) shows the distribution in the case-control study of the log-transformed calculated average concentrations of NO2 at the front door during the pregnancy period. Figure 1 (bottom) refers to the validation study and shows the calculated half-year average concentrations of NO2 at the front door plotted against the corresponding measured concentrations. For a given calculated value, the measured value has a 95 percent probability of being within the 95 percent prediction limits shown as dashed lines. The area between the prediction limits is divided into triangles (hatched) and hexagons (the remainder area) by the vertical and horizontal dotted lines, which indicate the cutoff points among the exposure groups. The area of the triangles, representing the misclassified observations, is smaller than that of the hexagons, representing the correctly classified observations. Table 6 shows the expected numbers of correctly classified and misclassified children in the case-control study under the assumption that the measured concentration at the front door is the exposure that is truly relevant to the hypothesis: 89 percent of the children categorized in the case-control study as having low exposure were expected to have been correctly categorized, 11 percent to be in the middle category, and none to be in the high or extreme category. Similarly, 83 percent, 80 percent, and 62 percent were expected to have been correctly classified in the middle, high, and extreme categories, respectively. Misclassification occurred only between adjacent categories.

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FIGURE 1. Distribution of exposure to NO2 in the case-control study (top) and calculated half-year average concentrations at the front door plotted against measured concentrations in the validation study (bottom), Denmark, 19681991. Rural areas are indicated by pluses and Copenhagen by squares, and the estimated line with 95% prediction limits (dashed lines) is drawn. The vertical dotted lines refer to the cutoff points among the exposure groups in the case-control study, and the horizontal dotted lines refer to the same percentiles in the estimated distribution of measured NO2 at the front door.
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TABLE 6. Expected misclassification among the four categories of exposure if calculated concentrations of NO2 are used as the surrogate for measured concentrations at the front door, Denmark, 19681991
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Table 7 shows that there would be more misclassification in the case-control study if the measured personal exposure to NO2 were assumed to be the truly relevant exposure, but misclassification was found mainly between adjacent categories.
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TABLE 7. Expected misclassification among the four categories of exposure if calculated concentrations of NO2 at the front door are used as the surrogate for measured personal exposure, Denmark, 19681991
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DISCUSSION
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We found no support for the hypothesis that traffic-related air pollution at the residence of children causes leukemias or central nervous system tumors, which are the two major diagnostic groups in children. The risk of lymphomas increased with increasing concentrations of ambient air pollution at the residence at the time the child was in utero, but the increase was restricted to Hodgkin's disease diagnosed before the age of 12 years.
The main finding of no effect conflicts with the results of previous studies. In a study in Denver, Colorado (2
), traffic density at the residence at the time of diagnosis was used as a surrogate for exposure. Eight percent of cases and 25 percent of controls did not respond, leaving 328 cases and 262 controls for the analyses. When exposure to more than 500 vehicles per day was compared with less exposure, the odds ratios were 1.7 for all cancers combined, 2.1 for leukemia, 1.7 for central nervous system tumors, and 0.7 for lymphomas. In a contrast of exposure to more than 10,000 and fewer than 500 vehicles per day, the odds ratios were 3.1 for all cancers combined and 4.7 for leukemia. The results for leukemia, central nervous system tumors, and all cancers combined were above the upper confidence limits found in our study (table 3). A Swedish group (3
) calculated the peak concentrations of NO2 (99th percentiles of 1-hour means) at the residences of 142 case children and 550 control children selected from a cohort of children with potential exposure to an electromagnetic field; only the exposure to NO2 at the latest address was considered. A comparison of children who lived at addresses with peak air pollution levels above the 75th percentile with those below the 50th percentile resulted in nonsignificantly elevated relative risks of 2.7, 2.7, and 5.1 for all cancers combined, leukemia, and central nervous system tumors. A study in West Midlands, United Kingdom (4
), found an incidence ratio of 1.16 based on 24 observed and 20.7 expected cases of leukemia among children living within 100 m of a main road. The exposure was assessed for the address at the time of the diagnosis. We designed our investigation to address the limitations of these studies, in particular the size of the study population, the selection procedures, and the exposure assessment.
The selection of cancer cases and control children from reliable, population-based registries makes selection bias in this study unlikely. Differential misclassification of exposure is also unlikely, because the data were provided by persons who were unaware of the identity or health status of the children and because the exposure assessment was based on all of the addresses occupied by the children, avoiding bias due to differential mobility of cases and controls.
The degree of nondifferential misclassification was estimated from the results of a validation study. Marshall et al. (19
) showed that nondifferential misclassification between adjacent categories of exposure, as expected in this study, can lead to risk estimates biased toward the neutral value; however, a true effect would be reduced only moderately by a 30 percent nondifferential misclassification of each of four exposure categories to each adjacent category. Moreover, the validation study showed that the misclassification or error (the difference between measured and calculated concentrations of NO2) was almost independent of the calculated concentration, as might be expected when exposure is predicted from a model (20
), and the error variance was constant. Thus, the data correspond to a "Berkson error model" (21
); trend estimates derived from exposure data encumbered with a "Berkson error" and constant error variance can be expected to be unbiased (22
, 23
). The measured values of NO2 in the validation study were approximately 0.81 times the calculated values. This has no implication for the trend or relative risk estimates, but the cutoff points between exposure groups (tables 4 and 5) should be multiplied by 0.81 to correspond to concentrations measured by the methods used in the validation study.
The validation study showed that greater misclassification of exposure occurred when measured personal exposure to NO2, rather than measured concentration at the front door, was considered to be the truly relevant exposure. This difference is due mainly to individual time-activity patterns combined with contributions to personal exposure from indoor sources and children's exposure to ambient air pollution at locations other than the residence. The relevance of the two types of measurement depends on the question to be answered. The major concern of families with small children, in relation to the hypothesis of this study, is whether their children are at risk of cancer because they live on a street with dense traffic. In this case, the measured concentration at the front door is the relevant choice, and the lower degree of misclassification would be relevant. Moreover, concentrations of NO2 at the front door reflect the concentrations of other traffic-related air pollutants as well. The higher degree of misclassification when personal measurements are considered to be the truly relevant exposure would pertain if the results of this study were used to evaluate whether exposure to NO2 (regardless of the source) causes cancer in children. As different air pollutants have different indoor sources, personal exposure to NO2 cannot be considered to indicate personal exposure to other (traffic-related) air pollutants by default. If a (group of) pollutant(s) present in traffic exhaust causes childhood cancer but traffic exhaust was not the main source of the exposure of children to this pollutant, it would be difficult to detect the effect by the methods used in this study. In that situation, however, the effect of overlooking a risk due partly to traffic would be limited exactly because traffic contributed only little to the exposure; in contrast, if traffic made a large contribution to the exposure of children to a relevant pollutant, one would have a better chance of detecting the effect by using the concentration at the front door as the exposure surrogate.
We have hitherto focused on the validity of calculated concentrations of NO2, but the levels of benzene were also addressed in the validation study, although fewer and only 1-week measurements were included. Despite a less precise measurement method for benzene (24
), simultaneous 1-week measurements of benzene and NO2 at the same 76 locations in Copenhagen showed that calculated concentrations were slightly more correlated with measured concentrations for benzene than for NO2 (11
), indicating a similar or better performance of the Operational Street Pollution Model when predicting concentrations of benzene in streets. Sources other than traffic at the residence may contribute significantly to children's personal exposure to benzene (24
, 25
), and use of the residential front-door concentration as a surrogate for personal exposure to benzene would probably imply a high degree of misclassification.
Altogether, the validation study indicated a low degree of misclassification of traffic-related air pollutants and a Berkson type of error if calculated levels are used as surrogate for measured levels outside the residence. However, because of different sources (other than traffic) of the personal exposure to different pollutants present in traffic exhaust, the results for misclassification of personal exposure to NO2 cannot be generalized, and the degree of misclassification of the personal exposure to other pollutants is unpredictable without validation for each pollutant.
Few risk factors have been consistently linked to the risks of leukemia, central nervous system tumors, and lymphomas in children; those that have are inherited genetic alterations, ionizing radiation, Epstein-Barr virus infection, age, and sex (26
). In our study, age, sex, and calendar period were excluded as confounders by matching, and it is difficult to imagine that inherited genetic alterations or exposure to diagnostic or therapeutic x-rays is associated with air pollution. Gamma-radiation from natural sources and indoor concentrations of radon vary by geographic region and type of house, but these were adjusted for in the analyses. Epstein-Barr virus is a cause of Burkitt's lymphoma in children, and these tumors constituted 20 percent of the non-Hodgkin's lymphomas. If exposure to Epstein-Barr virus is associated with air pollution at a residence, the most likely link would be urban development (many contacts) and not the number of vehicles passing by the address; urban development was adjusted for in the analyses. Since the degree of urban development and the concentration of ambient air pollution correlate, adjustment for urban development in the analyses might unduly remove a true effect of air pollution; however, the results of the unadjusted analyses excluded that possibility. The proposed risk factors that were not adjusted for in this study include medication, maternal smoking, parental occupation, pets, and immunizations. However, the evidence that these factors are indeed risk factors of childhood cancer is conflicting, and any increase in risk would be weak; moreover, strong correlations between these factors and traffic-related air pollution at residences are unlikely.
Given the low potential for selection bias, information bias, and confounding from known or proposed risk factors not adjusted for in the analyses and given the expected degree of nondifferential misclassification, the most reasonable interpretation of the results of our study is that no major risk of leukemia, central nervous system tumors, or all of the selected cancers combined is associated with traffic-related air pollution at the residence at the levels found in Denmark. The concentrations of benzene estimated in this study were similar to those found outdoors in the United States (25
). We are confident in this interpretation of no major risk as regards traffic-related air pollution at the residence, whereas an interpretation of no effect of personal exposure is problematic.
A causal interpretation of the association between the risk of Hodgkin's disease and exposure in utero is supported by the strength of the association, the exposure-response pattern, and previous findings of different risk factors of Hodgkin's disease in young and older children (27

30
). Moreover, immunologic disorders may be involved in the etiology of Hodgkin's disease (31
, 32
), and a number of studies indicate that exposure to ambient air pollution affects the human immune system (33

36
). Arguments against a causal interpretation are the absence of a known, plausible, specific biologic mechanism and the unexpected nature of the finding. Moreover, the finding was of only borderline significance in univariate models and may be a chance finding due to multiple testing.
In summary, traffic-related air pollution at the residence does not appear to cause leukemias, central nervous system tumors, or non-Hodgkin's lymphomas in children. The finding of a higher risk of Hodgkin's disease among children whose mothers had lived at residences with high outdoor levels of air pollution from traffic during the pregnancy might reflect a causal relation, although the evidence allows no firm conclusion at present.
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ACKNOWLEDGMENTS
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The study was supported by a grant from the Danish Environmental Research Program.
The authors are indebted to Dr. Ruwim Berkowicz, Elisabetta Vignati, Steen S. Jensen, and Dr. Henrik Skov at the National Environmental Research Institute and to Christian Lohse at the University of Odense for preparing the Operational Street Pollution Model for use in this study and for their support in the validation of the model.
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NOTES
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Reprint requests to Dr. Ole Raaschou-Nielsen, Danish Cancer Society, Institute of Cancer Epidemiology, Strandboulevarden 49, DK-2100 Copenhagen Ø, Denmark (e-mail: ole{at}cancer.dk).
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Received for publication March 8, 2000.
Accepted for publication June 12, 2000.