Background: For unknown reasons, the age-standardized incidence of testicular cancer has shown a rapid increase in virtually all countries (mostly Western) studied. For populations with a sufficiently long period of cancer registration, this development c

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Increase in Testicular Cancer Incidence in Six European Countries: a Birth Cohort Phenomenon

In this comparative study, we compensated for many of the known variables that influence children's growth and development by selecting two groups of 4-5-year-old Yaqui children who reside in the Yaqui Valley of northwestern Mexico. These children share similar genetic backgrounds, diets, water mineral contents, cultural patterns, and social behaviors. The major difference was their exposure to pesticides. Pesticides have been applied to the agricultural area of the valley since the late 1940s. In 1990, high levels of multiple pesticides were found in the cord blood of newborns and in breast milk. Building on anthropological methods for rapid rural appraisal of problems within the environment, a Rapid Assessment Tool for Preschool Children (RATPC) was developed to measure growth and development. The children of the agrarian region were compared to children living in the foothills, where pesticide use is avoided. The RATPC measured varied aspects of physical growth and abilities to perform, or function in, normal childhood activities. No differences were found in growth patterns. Functionally, the exposed children demonstrated decreases in stamina, gross and fine eye-hand coordination, 30-minute memory, and the ability to draw a person. The RATPC also pointed out areas in which more in-depth research on the toxicology of pesticides would be valuable.

An anthropological approach to the evaluation of preschool children exposed to pesticides in Mexico

Trends in cervical cancer incidence following the introduction of screening have mostly been studied using cross-sectional data and not analysed separately for squamous cell cancer and adenocarcinomas. Using Swedish nationwide data on incidence and mortality, we analysed trends during more than 3 decades and fitted Poisson-based age-period-cohort models, and also investigated whether screening has reduced the incidence of adenocarcinomas of the cervix. The incidence of reported cancer in situ increased rapidly during 1958-1967. Incidence rates of squamous cell cancer, fairly stable before 1968, decreased thereafter by 4-6% yearly in women aged 40-64, with a much smaller magnitude in younger and older women. An age-cohort model indicated a stable 70-75% reduction in incidence for women born 1940 and later compared with those born around 1923. The incidence of adenocarcinomas doubled during the 35-year study period. The mortality rate increased by 3.6% before 1968 and decreased by 4.0% yearly thereafter. Although a combination of organized and opportunistic screening can reduce the incidence of squamous cell cancer substantially, the incidence of adenocarcinomas appears uninfluenced by screening.

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Trends in cancer of the cervix uteri in Sweden following cytological screening.

Genome instability is a prerequisite for the development of cancer. It occurs when genome maintenance systems fail to safeguard the genome's integrity, whether as a consequence of inherited defects or induced via exposure to environmental agents (chemicals, biological agents and radiation). Thus, genome instability can be defined as an enhanced tendency for the genome to acquire mutations; ranging from changes to the nucleotide sequence to chromosomal gain, rearrangements or loss. This review raises the hypothesis that in addition to known human carcinogens, exposure to low dose of other chemicals present in our modern society could contribute to carcinogenesis by indirectly affecting genome stability. The selected chemicals with their mechanisms of action proposed to indirectly contribute to genome instability are: heavy metals (DNA repair, epigenetic modification, DNA damage signaling, telomere length), acrylamide (DNA repair, chromosome segregation), bisphenol A (epigenetic modification, DNA damage signaling, mitochondrial function, chromosome segregation), benomyl (chromosome segregation), quinones (epigenetic modification) and nano-sized particles (epigenetic pathways, mitochondrial function, chromosome segregation, telomere length). The purpose of this review is to describe the crucial aspects of genome instability, to outline the ways in which environmental chemicals can affect this cancer hallmark and to identify candidate chemicals for further study. The overall aim is to make scientists aware of the increasing need to unravel the underlying mechanisms via which chemicals at low doses can induce genome instability and thus promote carcinogenesis.

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Causes of genome instability: the effect of low dose chemical exposures in modern society

Interpretation of trends in disease rates using conventional age-period-cohort analyses is made difficult by the lack of a unique set of parameters specifying any given model. Because of difficulties inherent in age-period-cohort models, neither the magnitude nor the direction of a linear trend in birth cohort effects or calendar period effects can be determined unambiguously. This leads to considerable uncertainty in making inferences regarding disease etiology based on birth cohort or calendar period trends. In this paper, the authors demonstrate that changes in the direction or magnitude of long term trends can be identified unequivocally in age-period-cohort analyses, and they provide parametric methods for evaluating such changes in trend within the usual Poisson regression framework. Such changes can have important implications for disease etiology. This is demonstrated in applications of the proposed methods to the investigation of birth cohort trends in female breast cancer mortality rates obtained from the National Center for Health Statistics for the United States (1970-1989) and from the World Health Organization for Japan (1955-1979).

R. Bergstrom

Papers

Increasing cancer risk in younger birth cohorts in Sweden