Heinz Erich Wichmann

Bio: Heinz Erich Wichmann is an academic researcher from Ludwig Maximilian University of Munich. The author has contributed to research in topics: Population & Odds ratio. The author has an hindex of 69, co-authored 200 publications receiving 19887 citations. Previous affiliations of Heinz Erich Wichmann include Technische Universität München & Université de Montréal.

Radon in homes and risk of lung cancer: collaborative analysis of individual data from 13 European case-control studies.

Abstract: Objective To determine the risk of lung cancer associated with exposure at home to the radioactive disintegration products of naturally occurring radon gas Design Collaborative analysis of individual data from 13 case-control studies of residential radon and lung cancer. Setting Nine European countries. Subjects 7148 cases of lung cancer and 14 208 controls. Main outcome measures Relative risks of lung cancer and radon gas concentrations in homes inhabited during the previous 5-34 years measured in becquerels (radon disintegrations per second) per cubic metre (Bq/m 3 )o f household air. Results The mean measured radon concentration in homes of people in the control group was 97 Bq/m 3 , with 11% measuring > 200 and 4% measuring > 400 Bq/m 3 . For cases of lung cancer the mean concentration was 104 Bq/m 3 . The risk of lung cancer increased by 8.4% (95% confidence interval 3.0% to 15.8%) per 100 Bq/m 3 increase in measured radon (P = 0.0007). This corresponds to an increase of 16% (5% to 31%) per 100 Bq/m 3 increase in usual radon—that is, after correction for the dilution caused by random uncertainties in measuring radon concentrations. The dose-response relation seemed to be linear with no threshold and remained significant (P = 0.04) in analyses limited to individuals from homes with measured radon < 200 Bq/m 3 . The proportionate excess risk did not differ significantly with study, age, sex, or smoking. In the absence of other causes of death, the absolute risks of lung cancer by age 75 years at usual radon concentrations of 0, 100, and 400 Bq/m 3 would be about 0.4%, 0.5%, and 0.7%, respectively, for lifelong non-smokers, and about 25 times greater (10%, 12%, and 16%) for cigarette smokers. Conclusions Collectively, though not separately, these studies show appreciable hazards from residential radon, particularly for smokers and recent ex-smokers, and indicate that it is responsible for about 2% of all deaths from cancer in Europe.

Respiratory effects are associated with the number of ultrafine particles.

Abstract: The association between fine and ultrafine particles and respiratory health was studied in adults with a history of asthma in Erfurt, Eastern Germany. Twenty-seven nonsmoking asthmatics recorded their peak expiratory flow (PEF) and respiratory symptoms daily. The size distribution of ambient particles in the range of 0.01 to 2.5 microm was determined with an aerosol spectrometer during the winter season 1991-1992. Most of the particles (73%) were in the ultrafine fraction (smaller than 0.1 microm in diameter), whereas most of the mass (82%) was attributable to particles in the size range of 0.1 to 0.5 microm. Because these two fractions did not have similar time courses (correlation coefficient r = 0.51), a comparison of their health effects was possible. Both fractions were associated with a decrease of PEF and an increase in cough and feeling ill during the day. Health effects of the 5-d mean of the number of ultrafine particles were larger than those of the mass of the fine particles. In addition, the effects of the number of the ultrafine particles on PEF were stronger than those of particulate matter smaller than 10 microm (PM10). Therefore, the present study suggests that the size distribution of ambient particles helps to elucidate the properties of ambient aerosols responsible for health effects.

Tobacco and cancer: recent epidemiological evidence.

Abstract: During the 1950s, the evidence was clearly sufficient to establish the carcinogenicity of tobacco smoking (1). By the end of the 1950s, convincing evidence linking smoking with lung cancer and other cancers had been obtained from case–control and cohort studies, carcinogens had been identified in tobacco smoke, and cigarette smoke condensate had been shown to cause tumors when painted on the skin of mice. Since then, the numbers of deaths attributable to tobacco smoking have sharply increased, reflecting the heavy smoking patterns of previous decades. It has been estimated that tobacco smoking is currently responsible for approximately 30% of all cancer deaths in developed countries, and that if current smoking patterns persist, an epidemic of cancer attributable to tobacco smoking is expected to occur in developing countries (2). In addition, smoking causes even more deaths from vascular, respiratory, and other diseases than from cancer, so that, in total, tobacco smoking is estimated to account for approximately 4–5 million deaths a year worldwide. This number is projected to increase to approximately 10 million a year by 2030. Thus, if current smoking patterns continue, there will be more than 1 billion deaths attributable to tobacco smoking in the 21 century compared with approximately 100 million deaths in the 20 century (2). The only other causes of disease with such rapidly increasing impact are those associated with human immunodeficiency virus infection and, perhaps, obesity in Western countries (2). In this commentary, we review the evidence regarding the carcinogenicity of tobacco smoke that has accumulated during the last 16 years since the publication of Monograph 38 of the International Agency for Research on Cancer (IARC) in 1986 (3) to the updating of that monograph (Monograph 83) in 2002 (4). The evidence now available shows that tobacco smoke is a multipotent carcinogenic mixture that can cause cancer in many different organs. In addition, exposure to secondhand tobacco smoke (i.e., involuntary or passive smoking by persons who do not smoke) is also carcinogenic for the human lung. This commentary, written by the epidemiologists who participated in the 2002 IARC Working Group for the preparation of the IARC Monograph 83 (4), is based on the substantial body of evidence reviewed for that purpose. It represents, however, solely the views of the authors.

KORA--a research platform for population based health research.

Abstract: KORA (Cooperative Health Research in the Region Augsburg) is a regional research platform for population-based surveys and subsequent follow-up studies in the fields of epidemiology, health economics, and health care research. KORA was established in 1996 to continue and expand the MONICA project in Augsburg, including the Acute Myocardial Infarction (AMI) Registry. The available pool of study participants allows for cohort, case-control and family studies. We present the KORA infrastructure, aspects of data management and quality control, and the concept of cooperative research. The increasing use of the MONICA/KORA cohorts for a variety of research topics, with a recent focus on genetic epidemiology, indicates the attractiveness of this concept.

IARC Monographs on the Evaluation of Carcinogenic Risks to Humans

Abstract: Viral hepatitis in all its forms is a major public health problem throughout the world, affecting several hundreds of millions of people. Viral hepatitis is a cause of considerable morbidity and mortality both from acute infection and chronic sequelae which include, in the case of hepatitis B, C and D, chronic active hepatitis and cirrhosis. Hepatocellular carcinoma, which is one of the 10 commonest cancers worldwide, is closely associated with hepatitis B and, at least in some regions of the world, with hepatitis C virus. This timely monograph is a distillation of knowledge of hepatitis B, C and D, based on a review of 1000 studies by a small group of scientists. (It is interesting to note in passing that some 5000 papers on viral hepatitis are published annually in the world literature.) The epidemiological, clinical and experimental data on the association between infection with hepatitis B virus and primary liver cancer in humans are reviewed in a readable and succinct format. The available information on hepatitis C and progression to chronic infection is also evaluated and it is concluded (perhaps a little prematurely) that hepatitis C virus is carcinogenic. However, it is concluded that hepatitis D virus, an unusual virus with a number of similarities to certain plant viral satellites and viroids, cannot be classified as a human carcinogen. There are some minor criticisms: there are few illustrations and some complex tabulations (for example, Table 6) and no subject index. A cumulative cross index to IARC Monographs is of little value and occupies nearly 30 pages. This small volume is a useful addition to the overwhelming literature on viral hepatitis, and the presentation is similar to the excellent World Health Organisation Technical Reports series on the subject published in the past. It is strongly recommended as a readable up-to-date summary of a complex subject; and at a cost of 65 Sw.fr (approximately £34) is excellent value. A J ZUCKERMAN

Nanotoxicology: An Emerging Discipline Evolving from Studies of Ultrafine Particles

Abstract: Although humans have been exposed to airborne nanosized particles (NSPs; < 100 nm) throughout their evolutionary stages, such exposure has increased dramatically over the last century due to anthropogenic sources. The rapidly developing field of nanotechnology is likely to become yet another source through inhalation, ingestion, skin uptake, and injection of engineered nanomaterials. Information about safety and potential hazards is urgently needed. Results of older bio-kinetic studies with NSPs and newer epidemiologic and toxicologic studies with airborne ultrafine particles can be viewed as the basis for the expanding field of nanotoxicology, which can be defined as safety evaluation of engineered nanostructures and nanodevices. Collectively, some emerging concepts of nanotoxicology can be identified from the results of these studies. When inhaled, specific sizes of NSPs are efficiently deposited by diffusional mechanisms in all regions of the respiratory tract. The small size facilitates uptake into cells and transcytosis across epithelial and endothelial cells into the blood and lymph circulation to reach potentially sensitive target sites such as bone marrow, lymph nodes, spleen, and heart. Access to the central nervous system and ganglia via translocation along axons and dendrites of neurons has also been observed. NSPs penetrating the skin distribute via uptake into lymphatic channels. Endocytosis and biokinetics are largely dependent on NSP surface chemistry (coating) and in vivo surface modifications. The greater surface area per mass compared with larger-sized particles of the same chemistry renders NSPs more active biologically. This activity includes a potential for inflammatory and pro-oxidant, but also antioxidant, activity, which can explain early findings showing mixed results in terms of toxicity of NSPs to environmentally relevant species. Evidence of mitochondrial distribution and oxidative stress response after NSP endocytosis points to a need for basic research on their interactions with subcellular structures. Additional considerations for assessing safety of engineered NSPs include careful selections of appropriate and relevant doses/concentrations, the likelihood of increased effects in a compromised organism, and also the benefits of possible desirable effects. An interdisciplinary team approach (e.g., toxicology, materials science, medicine, molecular biology, and bioinformatics, to name a few) is mandatory for nanotoxicology research to arrive at an appropriate risk assessment.

Biological insights from 108 schizophrenia-associated genetic loci

Abstract: Schizophrenia is a highly heritable disorder. Genetic risk is conferred by a large number of alleles, including common alleles of small effect that might be detected by genome-wide association studies. Here we report a multi-stage schizophrenia genome-wide association study of up to 36,989 cases and 113,075 controls. We identify 128 independent associations spanning 108 conservatively defined loci that meet genome-wide significance, 83 of which have not been previously reported. Associations were enriched among genes expressed in brain, providing biological plausibility for the findings. Many findings have the potential to provide entirely new insights into aetiology, but associations at DRD2 and several genes involved in glutamatergic neurotransmission highlight molecules of known and potential therapeutic relevance to schizophrenia, and are consistent with leading pathophysiological hypotheses. Independent of genes expressed in brain, associations were enriched among genes expressed in tissues that have important roles in immunity, providing support for the speculated link between the immune system and schizophrenia.