Background: Environmental health effects vary considerably with regard to their severity, type of disease, and duration. Integrated measures of population health, such as environmental burden of disease (EBD), are useful for setting priorities in environmental health policies and research. This review is a summary of the full Environmental Burden of Disease in European countries (EBoDE) project report. Objectives: The EBoDE project was set up to provide assessments for nine environmental risk factors relevant in selected European countries (Belgium, Finland, France, Germany, Italy, and the Netherlands). Methods: Disability-adjusted life years (DALYs) were estimated for benzene, dioxins, secondhand smoke, formaldehyde, lead, traffic noise, ozone, particulate matter (PM2.5), and radon, using primarily World Health Organization data on burden of disease, (inter)national exposure data, and epidemiological or toxicological risk estimates. Results are presented here without discounting or age-weighting. Results: About 3–7% of the annual burden of disease in the participating countries is associated with the included environmental risk factors. Airborne particulate matter (diameter ≤ 2.5 μm; PM2.5) is the leading risk factor associated with 6,000–10,000 DALYs/year and 1 million people. Secondhand smoke, traffic noise (including road, rail, and air traffic noise), and radon had overlapping estimate ranges (600–1,200 DALYs/million people). Some of the EBD estimates, especially for dioxins and formaldehyde, contain substantial uncertainties that could be only partly quantified. However, overall ranking of the estimates seems relatively robust. Conclusions: With current methods and data, environmental burden of disease estimates support meaningful policy evaluation and resource allocation, including identification of susceptible groups and targets for efficient exposure reduction. International exposure monitoring standards would enhance data quality and improve comparability. Citation: Hänninen O, Knol AB, Jantunen M, Lim TA, Conrad A, Rappolder M, Carrer P, Fanetti AC, Kim R, Buekers J, Torfs R, Iavarone I, Classen T, Hornberg C, Mekel OC, EBoDE Working Group. 2014. Environmental burden of disease in Europe: assessing nine risk factors in six countries. Environ Health Perspect 122:439–446; http://dx.doi.org/10.1289/ehp.1206154

SHP-2 is a protein tyrosine phosphatase functioning as signal transducer downstream to growth factor and cytokine receptors. SHP-2 is required during development, and germline mutations in PTPN11, the gene encoding SHP-2, cause Noonan syndrome. SHP-2 plays a crucial role in hematopoietic cell development. We recently demonstrated that somatic PTPN11 mutations are the most frequent lesion in juvenile myelomonocytic leukemia and are observed in a smaller percentage of children with other myeloid malignancies. Here, we report that PTPN11 lesions occur in childhood acute lymphoblastic leukemia (ALL). Mutations were observed in 23 of 317 B-cell precursor ALL cases, but not among 44 children with T-lineage ALL. In the former, lesions prevalently occurred in TEL-AML1^- cases with CD19⁺/CD10⁺/cyIgM^- immunophenotype. PTPN11, NRAS, and KRAS2 mutations were largely mutually exclusive and accounted for one third of common ALL cases. We also show that, among 69 children with acute myeloid leukemia, PTPN11 mutations occurred in 4 of 12 cases with acute monocytic leukemia (FAB-M5). Leukemia-associated PTPN11 mutations were missense and were predicted to result in SHP-2 gain-of-function. Our findings provide evidence for a wider role of PTPN11 lesions in leukemogenesis, but also suggest a lineage-related and differentiation stage-related contribution of these lesions to clonal expansion. (Blood. 2004;104:307-313)

The very rapid worldwide increase in mobile phone use in the last decade has generated considerable interest in the possible health effects of exposure to radio frequency (RF) fields. A multinational case–control study, INTERPHONE, was set-up to investigate whether mobile phone use increases the risk of cancer and, more specifically, whether the RF fields emitted by mobile phones are carcinogenic. The study focused on tumours arising in the tissues most exposed to RF fields from mobile phones: glioma, meningioma, acoustic neurinoma and parotid gland tumours. In addition to a detailed history of mobile phone use, information was collected on a number of known and potential risk factors for these tumours. The study was conducted in 13 countries. Australia, Canada, Denmark, Finland, France, Germany, Israel, Italy, Japan, New Zealand, Norway, Sweden, and the UK using a common core protocol. This paper describes the study design and methods and the main characteristics of the study population. INTERPHONE is the largest case–control study to date investigating risks related to mobile phone use and to other potential risk factors for the tumours of interest and includes 2,765 glioma, 2,425 meningioma, 1,121 acoustic neurinoma, 109 malignant parotid gland tumour cases and 7,658 controls. Particular attention was paid to estimating the amount and direction of potential recall and participation biases and their impact on the study results.

BASAL CELL carcinoma (BCC) is the most common cancer in white populations. Approximately 1 million cases of basal and squamous cell skin cancers were expected to be diagnosed in 1999 in the United States.¹ Although mortality from BCC is low, due to an extremely low metastatizing potential (estimated around 0.1%),² this tumor carries considerable morbidity and costs for health care services.³

Background: Adverse health effects at relatively low levels of ambient air pollution have consistently been reported in the last years. We conducted a time-series panel study of subjects with chronic obstructive pulmonary disease (COPD), asthma, and ischemic heart disease (IHD) to evaluate whether daily levels of air pollutants have a measurable impact on the lung function of adult subjects with pre-existing lung or heart diseases.Methods: Twenty-nine patients with COPD, asthma, or IHD underwent repeated lung function tests by supervised spirometry in two one-month surveys. Daily samples of coarse (PM_10–2.5) and fine (PM_2.5) particulate matter were collected by means of dichotomous samplers, and the dust was gravimetrically analyzed. The particulate content of selected metals (cadmium, chrome, iron, nickel, lead, platinum, vanadium, and zinc) was determined by atomic absorption spectrometry. Ambient concentrations of nitrogen dioxide (NO₂), carbon monoxide (CO), ozone (O₃), and sulphur dioxide (SO₂) were obtained from the regional air-quality monitoring network. The relationships between concentrations of air pollutants and lung function parameters were analyzed by generalized estimating equations (GEE) for panel data.Results: Decrements in lung function indices (FVC and/or FEV₁) associated with increasing concentrations of PM_2.5, NO₂and some metals (especially zinc and iron) were observed in COPD cases. Among the asthmatics, NO₂was associated with a decrease in FEV₁. No association between average ambient concentrations of any air pollutant and lung function was observed among IHD cases.Conclusion: This study suggests that the short-term negative impact of exposure to air pollutants on respiratory volume and flow is limited to individuals with already impaired respiratory function. The fine fraction of ambient PM seems responsible for the observed effects among COPD cases, with zinc and iron having a potential role via oxidative stress. The respiratory function of the relatively young and mild asthmatics included in this study seems to worsen when ambient levels of NO₂increase.

Background: Chronic diseases are increasing among children in Latin America. Objective and Methods: To examine environmental risk factors for chronic disease in Latin American children and to develop a strategic initiative for control of these exposures, the World Health Organization (WHO) including the Pan American Health Organization (PAHO), the Collegium Ramazzini, and Latin American scientists reviewed regional and relevant global data. Results: Industrial development and urbanization are proceeding rapidly in Latin America, and environmental pollution has become widespread. Environmental threats to children’s health include traditional hazards such as indoor air pollution and drinking-water contamination; the newer hazards of urban air pollution; toxic chemicals such as lead, asbestos, mercury, arsenic, and pesticides; hazardous and electronic waste; and climate change. The mix of traditional and modern hazards varies greatly across and within countries reflecting industrialization, urbanization, and socioeconomic forces. Conclusions: To control environmental threats to children’s health in Latin America, WHO, including PAHO, will focus on the most highly prevalent and serious hazards—indoor and outdoor air pollution, water pollution, and toxic chemicals. Strategies for controlling these hazards include developing tracking data on regional trends in children’s environmental health (CEH), building a network of Collaborating Centres, promoting biomedical research in CEH, building regional capacity, supporting development of evidence-based prevention policies, studying the economic costs of chronic diseases in children, and developing platforms for dialogue with relevant stakeholders. Citation: Laborde A, Tomasina F, Bianchi F, Bruné MN, Buka I, Comba P, Corra L, Cori L, Duffert CM, Harari R, Iavarone I, McDiarmid MA, Gray KA, Sly PD, Soares A, Suk WA, Landrigan PJ. 2015. Children’s health in Latin America: the influence of environmental exposures. Environ Health Perspect 123:201–209; http://dx.doi.org/10.1289/ehp.1408292