Exposure to benzene increases the risk for acute myeloid leukemia and possibly other types of cancer in adults. For children, only limited evidence about benzene and cancer exists. A few studies have ...indicated that benzene may increase risk for some subtypes of childhood cancer but not for others. We aimed to investigate if outdoor levels of benzene at the residence increase the risk for subtypes of leukemia, lymphoma and CNS tumor in children. We identified 1,989 children diagnosed with leukemia, lymphoma or CNS tumor during 1968–1991 in the Danish Cancer Registry and randomly selected 5,506 control children from the Danish population, matched on sex, age and calendar time. We traced residential history of all children from 9 months before birth to time of diagnosis, calculated outdoor benzene concentration at all addresses and summarized cumulative exposure over fetal and childhood periods separately. We used conditional logistic regression for the statistical analyses. Benzene exposure during childhood above the 90th percentile was associated with relative risks for acute lymphocytic leukemia (ALL) and acute myeloid leukemia (AML) of 1.0 (95% confidence intervals (CI): 0.6–1.7) and 1.9 (95% CI: 0.3–11.1), respectively, when compared with exposure levels below the median. For CNS tumors, there was a tendency of lower risk for ependymoma and higher risk for medulloblastoma in association with higher exposure. In conclusion, benzene was associated with higher risk for childhood AML, but not ALL, which is consistent with the few previous studies.
What's new?
Benzene is classified as a human carcinogen causing acute myeloid leukemia (AML) in adults exposed to relatively high concentrations at work. It is, however, uncertain whether low concentrations of benzene in outdoor air causes leukemia in children. In this population‐based case–control study, the authors found an association between risk for acute myeloid leukemia—but not acute lymphocytic leukemia (ALL)—in children and benzene concentration outside their residence. The results are in line with the few previous studies examining exposure to outdoor benzene and risk for AML in children.
The aetiology of childhood leukaemia is poorly understood. Knowledge about differences in risk by socioeconomic status (SES) may enhance etiologic insights. We conducted a nationwide register‐based ...case‐control study to evaluate socioeconomic differences in the risk of childhood leukaemia in Denmark and to access whether associations varied by different measures of SES, time point of assessment, leukaemia type and age at diagnosis. We identified all cases of leukaemia in children aged 0 to 19 years, born and diagnosed between 1980 and 2013 from the Danish Cancer Registry (N = 1336) and sampled four individually matched controls per case (N = 5330). We used conditional logistic regression models for analysis. Medium and high level of parental education was associated with a higher risk of acute myeloid leukaemia (AML) in the offspring, mainly driven by children diagnosed at ages 0 to 4 years odds ratio (OR) for high maternal education = 3.07; 95% confidence interval (CI): 1.44‐6.55. We also observed a modestly increased risk for lymphoid leukaemia (LL) in association with higher level of parental education, but only in children diagnosed at ages 5 to 19 years. Higher parental income was associated with an increased risk of LL but not AML among children aged 5 to 19 years at diagnosis (OR for high maternal income = 2.78; 95% CI: 1.32‐5.89). Results for neighbourhood SES measures indicated null associations. Bias or under‐ascertainment of cases among families with low income or basic education are unlikely to explain the observed socioeconomic differences. Future research addressing explicitly the underlying mechanisms of our results may help to enhance etiologic insights of the disease.
What's new?
The aetiology of childhood leukaemia is still poorly understood. In this nationwide register‐based case‐control study, the authors found that higher level of parental education was associated with higher risk of childhood leukaemia in Denmark, particularly acute myeloid leukaemia. Higher parental income was also associated with an increased risk of lymphoid leukaemia, but only among children aged 5‐19 years. Bias or under‐ascertainment of cases among families with low income or basic education are unlikely to explain the observed socioeconomic differences. Identifying differences in the risk of childhood leukaemia by socioeconomic group may help to generate new etiologic hypotheses, which are urgently needed for developing prevention strategies.
There is limited evidence regarding a possible association between exposure to ambient air pollutants and the risk of non‐Hodgkin lymphoma (NHL). Previous epidemiological studies have relied on crude ...estimations for air pollution exposure and/or small numbers of NHL cases. The objective of our study was to analyze this association based on air pollution modeled at the address level and NHL cases identified from the nationwide Danish Cancer Registry. We identified 20,874 incident NHL cases diagnosed between 1989 and 2014 and randomly selected 41,749 controls matched on age and gender among the entire Danish population. We used conditional logistic regression to estimate odds ratios (ORs) and adjusted for individual and neighborhood level sociodemographic variables. There was no association between exposure to PM2.5, BC, O3, SO2 or NO2 and overall risk of NHL but several air pollutants were associated with higher risk of follicular lymphoma, but statistically insignificant, for example, PM2.5 (OR = 1.15 per 5 μg/m3; 95% CI: 0.98–1.34) and lower risk for diffuse large B‐cell lymphoma (OR = 0.92 per 5 μg/m3; 95% CI: 0.82–1.03). In this population‐based study, we did not observe any convincing evidence of a higher overall risk for NHL with higher exposure to ambient air pollutants.
What's new?
Known risk factors of non‐Hodgkin lymphoma (NHL) appear to be involved in only a small percentage of NHL cases. However, while other factors are suspected of influencing NHL risk, including socioeconomic factors and outdoor air pollution, existing evidence is inconclusive. In this investigation of outdoor air pollution and NHL risk in NHL patients diagnosed between 1989 and 2014 in Denmark, no association was detected between long‐term air pollution exposure at an individual's residence and overall NHL risk. Air pollution was insignificantly associated with increased risk of follicular lymphoma and reduced risk of diffuse large B‐cell lymphoma, two common NHL subtypes.
Exposure to traffic-related air pollutants is an important public health issue. Here, we present a systematic review and meta-analysis of research examining the relationship of measures of nitrogen ...oxides (NOx) and of various measures of traffic-related air pollution exposure with lung cancer.
We conducted random-effects meta-analyses of studies examining exposure to nitrogen dioxide (NO2) and NOx and its association with lung cancer. We identified 20 studies that met inclusion criteria and provided information necessary to estimate the change in lung cancer per 10-μg/m3 increase in exposure to measured NO2. Further, we qualitatively assessed the evidence of association between distance to roadways and traffic volume associated with lung cancer.
The meta-estimate for the change in lung cancer associated with a 10-μg/m3 increase in exposure to NO2 was 4% (95% CI: 1%, 8%). The meta-estimate for change in lung cancer associated with a 10-μg/m3 increase in NOx was similar and slightly more precise, 3% (95% CI: 1%, 5%). The NO2 meta-estimate was robust to different confounding adjustment sets as well as the exposure assessment techniques used. Trim-and-fill analyses suggest that if publication bias exists, the overall meta-estimate is biased away from the null. Forest plots for measures of traffic volume and distance to roadways largely suggest a modest increase in lung cancer risk.
We found consistent evidence of a relationship between NO2, as a proxy for traffic-sourced air pollution exposure, with lung cancer. Studies of lung cancer related to residential proximity to roadways and NOx also suggest increased risk, which may be attributable partly to air pollution exposure. The International Agency for Research on Cancer recently classified outdoor air pollution and particulate matter as carcinogenic (Group 1). These meta-analyses support this conclusion, drawing particular attention to traffic-sourced air pollution.
Hamra GB, Laden F, Cohen AJ, Raaschou-Nielsen O, Brauer M, Loomis D. 2015. Lung cancer and exposure to nitrogen dioxide and traffic: a systematic review and meta-analysis. Environ Health Perspect 123:1107-1112; http://dx.doi.org/10.1289/ehp.1408882.
Summary Background Ambient air pollution is suspected to cause lung cancer. We aimed to assess the association between long-term exposure to ambient air pollution and lung cancer incidence in ...European populations. Methods This prospective analysis of data obtained by the European Study of Cohorts for Air Pollution Effects used data from 17 cohort studies based in nine European countries. Baseline addresses were geocoded and we assessed air pollution by land-use regression models for particulate matter (PM) with diameter of less than 10 μm (PM10 ), less than 2·5 μm (PM2·5 ), and between 2·5 and 10 μm (PMcoarse ), soot (PM2·5absorbance ), nitrogen oxides, and two traffic indicators. We used Cox regression models with adjustment for potential confounders for cohort-specific analyses and random effects models for meta-analyses. Findings The 312 944 cohort members contributed 4 013 131 person-years at risk. During follow-up (mean 12·8 years), 2095 incident lung cancer cases were diagnosed. The meta-analyses showed a statistically significant association between risk for lung cancer and PM10 (hazard ratio HR 1·22 95% CI 1·03–1·45 per 10 μg/m3 ). For PM2·5 the HR was 1·18 (0·96–1·46) per 5 μg/m3 . The same increments of PM10 and PM2·5 were associated with HRs for adenocarcinomas of the lung of 1·51 (1·10–2·08) and 1·55 (1·05–2·29), respectively. An increase in road traffic of 4000 vehicle-km per day within 100 m of the residence was associated with an HR for lung cancer of 1·09 (0·99–1·21). The results showed no association between lung cancer and nitrogen oxides concentration (HR 1·01 0·95–1·07 per 20 μg/m3 ) or traffic intensity on the nearest street (HR 1·00 0·97–1·04 per 5000 vehicles per day). Interpretation Particulate matter air pollution contributes to lung cancer incidence in Europe. Funding European Community's Seventh Framework Programme.
Purpose
Differences in the risk of childhood central nervous system (CNS) tumors by socioeconomic status (SES) may enhance etiologic insights. We conducted a nationwide register-based case–control ...study to evaluate socioeconomic differences in the risk of childhood CNS tumors in Denmark and examined whether associations varied by different SES measures, time points of assessment, specific tumor types, and age at diagnosis.
Methods
We identified all children born between 1981 and 2013 and diagnosed with a CNS tumor at ages 0–19 years (
n
= 1,273) from the Danish Cancer Registry and sampled four individually matched controls per case (
n
= 5,086). We used conditional logistic regression models to estimate associations with individual-level and neighborhood-level socioeconomic measures.
Results
We observed elevated risks of ependymoma and embryonal CNS tumors in association with higher parental education (odds ratios (ORs) of 1.6–2.1 for maternal or paternal high education and ependymoma) and higher risk of all tumor types in association with higher maternal income, e.g., OR 1.93; 95% CI 1.05–3.52 for high versus low income for astrocytoma and other gliomas. Associations were often stronger in children diagnosed at ages 5–19 years. We found little evidence for an association with neighborhood SES.
Conclusion
This large nationwide register study with minimal risk of bias showed that having parents with higher educational level and a mother with higher income was associated with a higher risk of childhood CNS tumors. Bias or under-ascertainment of cases among families with low income or basic education is unlikely to explain our findings.
Background: Particulate matter (PM) in outdoor air pollution was recently designated a Group I carcinogen by the International Agency for Research on Cancer (IARC). This determination was based on ...the evidence regarding the relationship of PM2.5 and PM10 to lung cancer risk; however, the IARC evaluation did not include a quantitative summary of the evidence. Objective: Our goal was to provide a systematic review and quantitative summary of the evidence regarding the relationship between PM and lung cancer. Methods: We conducted meta-analyses of studies examining the relationship of exposure to PM2.5 and PM10 with lung cancer incidence and mortality. In total, 18 studies met our inclusion criteria and provided the information necessary to estimate the change in lung cancer risk per 10- mu g/m3 increase in exposure to PM. We used random-effects analyses to allow between-study variability to contribute to meta-estimates. Results: The meta-relative risk for lung cancer associated with PM2.5 was 1.09 (95% CI: 1.04, 1.14). The meta-relative risk of lung cancer associated with PM10 was similar, but less precise: 1.08 (95% CI: 1.00, 1.17). Estimates were robust to restriction to studies that considered potential confounders, as well as subanalyses by exposure assessment method. Analyses by smoking status showed that lung cancer risk associated with PM2.5 was greatest for former smokers 1.44 (95% CI: 1.04, 2.01), followed by never-smokers 1.18 (95% CI: 1.00, 1.39), and then current smokers 1.06 (95% CI: 0.97, 1.15). In addition, meta-estimates for adenocarcinoma associated with PM2.5 and PM10 were 1.40 (95% CI: 1.07, 1.83) and 1.29 (95% CI: 1.02, 1.63), respectively. Conclusion: The results of these analyses, and the decision of the IARC Working Group to classify PM and outdoor air pollution as carcinogenic (Group 1), further justify efforts to reduce exposures to air pollutants that can arise from many sources.
Exposure to traffic noise may result in stress and sleep disturbances. Studies on self‐reported sleep duration and breast cancer risk have found inconsistent results. In a population‐based Danish ...cohort of 29,875 women aged 50–64 years at enrolment in 1993–1997, we identified 1219 incident, postmenopausal breast cancer cases during follow‐up through 2010. Mean follow‐up time was 12.3 years. Road traffic and railway noise was calculated for all present and historical residential addresses from 1987 to 2010. We used Cox proportional hazard model for analyses and adjusted for hormone replacement therapy use, parity, alcohol consumption and other potential confounders. We found no overall association between residential road traffic or railway noise and breast cancer risk. Among women with estrogen receptor negative breast cancer, a 10‐dB higher level of road traffic noise (continuous scale) during the previous 1, 5 and 10 years were associated with 28% (95% CI: 1.04–1.56), 23% (95% CI: 1.00–1.51) and 20% (95% CI: 0.97–1.48) higher risks of estrogen receptor negative breast cancer, respectively, in fully adjusted models. Similarly, a 10‐dB increase in railway noise (1‐year mean at diagnosis address) increased risk for estrogen receptor negative breast cancer by 38% (95% CI: 1.01–1.89). There was no association between road traffic or railway noise and estrogen receptor positive breast cancer. In conclusion, these results suggest that residential road traffic and railway noise may increase risk of estrogen receptor negative breast cancer. As the first study on traffic noise and breast cancer results should be treated with caution.
What's new?
Urbanization is linked to increased traffic noise, exposure to which is associated with stress and sleep disturbances. However, the impact of sleep duration and traffic noise exposure on breast cancer risk remains unclear. The present study suggests that residential exposure to road traffic and railway noise is associated with a dose‐dependent increase in risk for estrogen receptor negative breast cancer. Exposure to road traffic and railway noise is considerable in many parts of the world, including the European Union, where more than 30% of the population is exposed to road traffic noise at levels exceeding WHO guideline values.
Particulate matter (PM) in outdoor air pollution was recently designated a Group I carcinogen by the International Agency for Research on Cancer (IARC). This determination was based on the evidence ...regarding the relationship of PM2.5 and PM10 to lung cancer risk; however, the IARC evaluation did not include a quantitative summary of the evidence.
Our goal was to provide a systematic review and quantitative summary of the evidence regarding the relationship between PM and lung cancer.
We conducted meta-analyses of studies examining the relationship of exposure to PM2.5 and PM10 with lung cancer incidence and mortality. In total, 18 studies met our inclusion criteria and provided the information necessary to estimate the change in lung cancer risk per 10-μg/m3 increase in exposure to PM. We used random-effects analyses to allow between-study variability to contribute to meta-estimates.
The meta-relative risk for lung cancer associated with PM2.5 was 1.09 (95% CI: 1.04, 1.14). The meta-relative risk of lung cancer associated with PM10 was similar, but less precise: 1.08 (95% CI: 1.00, 1.17). Estimates were robust to restriction to studies that considered potential confounders, as well as subanalyses by exposure assessment method. Analyses by smoking status showed that lung cancer risk associated with PM2.5 was greatest for former smokers 1.44 (95% CI: 1.04, 1.22), followed by never-smokers 1.18 (95% CI: 1.00, 1.39), and then current smokers 1.06 (95% CI: 0.97, 1.15). In addition, meta-estimates for adenocarcinoma associated with PM2.5 and PM10 were 1.40 (95% CI: 1.07, 1.83) and 1.29 (95% CI: 1.02, 1.63), respectively.
The results of these analyses, and the decision of the IARC Working Group to classify PM and outdoor air pollution as carcinogenic (Group 1), further justify efforts to reduce exposures to air pollutants that can arise from many sources.
The integrated model system DEHM/UBM/AirGIS, developed at Aarhus University, Department of Environmental Science, has been extended with the dynamic aerosol module M7 to account for particle number ...concentrations of particles with diameters below 1 μm in the atmosphere. The aim of this development is to quantify the spatial and temporal distribution of particle number concentration across Denmark and evaluate the results with available measurements. This article presents model results for particle number concentrations from the regional scale model DEHM and the urban scale model UBM, for comparison with measurements of particle number concentrations from European and Danish measurement stations. The deterministic modelling of particle number concentration has been vitiated by the lack of consistency between emission inventories, and the evaluation of the models is challenged by the lack of consistent long-term measurements data. The performance evaluation of the DEHM and UBM models shows that both models overestimate the level of the particle number concentrations at all stations, however, the results for the correlation coefficients are 0.86 for DEHM and in the range from 0.86 to 0.87, for UBM, for annual mean particle number concentrations at Danish measurement stations. We conclude that the inclusion of particle number concentration in DEHM and UBM shows some capability of reproducing observed patterns, when comparing the results of the models with available measurements, but that there is also room for improvement, especially with respect to the emission inventories and preprocessing of emissions and to the treatment of volatile organic compounds based on natural emissions during summer time.
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