Occupational health of semiconductor workers has been the subject of only a few, limited investigations, all in developed countries. Findings of reproductive problems and increased risk of several cancers have not been adequately followed up by larger, more definitive studies. Industry and government have failed to take the initiative to protect workers before the industry was exported to many regions of the world. There is a compelling need for a large, international epidemiologic study of the semiconductor industry and its workforce. Eur. J. Oncol., 14 (2), 69-78, 2009

The Finnish Institute of Occupational Health (FIOH) has received support from the World Health Organization (WHO) and the International Labor Office (ILO) to publish the African Newsletter on Occupational Health and Safety. The African Newsletter on Occupational Health and Safety should not be a medium for industry propaganda, or the source of misinformation among the workers of Africa. Instead, FIOH should provide the same level of scientific information in Africa that it does in Finland and other developed countries.

We conducted a mortality time series study to investigate the association between daily mortality for congestive heart failure (CHF), and daily concentrations of particles and gaseous pollutants in the ambient air of Montreal, Quebec, during the period 1984–1993. In addition, using data from the universal Quebec Health Insurance Plan, we identified individuals ⩾65 years of age who, one year before death, had a diagnosis of CHF. Fixed-site air pollution monitors in Montreal provided daily mean levels of pollutants. We regressed the logarithm of daily counts of mortality on the daily mean levels of each pollutant, after accounting for seasonal and subseasonal fluctuations in the mortality time series, non-Poisson dispersion, weather variables, and other gaseous and particle pollutants. Using cause of death information, we did not find any associations between daily mortality for CHF and any air pollutants. The analyses of CHF defined from the medical record showed positive associations with coefficient of haze, the extinction coefficient, SO2, and NO2. For example, the mean percent increase in daily mortality for an increase in the coefficient of haze across the interquartile range was 4.32% (95% CI: 0.95–7.80%) and for NO2 it was 4.08% (95% CI: 0.59–7.68%). These effects were generally higher in the warm season.

The Japanese have the longest lifespan worldwide, but this has been mostly due to reductions in the mortality rates from diseases other than malignant neoplasms. Changes in the age-adjusted mortality rates (AMRs) for malignant neoplasms in Japan from 1950 to 2000 are analyzed to elucidate the overall trend. The overall AMRs for all malignant neoplasms in men increased from 1950 to 2000, and decreased slowly in women during the same period. Changes since 1990 have been small in both genders, but show a hopeful trend towards a decrease in the total AMR since 1995. These trends reflect a balance between the decreased AMR from gastric (both male and female) and uterine cancers and increases in many other malignant neoplasms. However, in the period 1990–2000, the decrease in the AMR from gastric and uterine cancers has shown a trend towards leveling off. Therefore, improving the trend towards reductions in cancer incidence and mortality in the 21st century and beyond will depend on achieving changes in other cancer sites, which can only be realized through the twofold approach of preventative medicine and research as well as improvements in the levels of diagnosis and therapy. Much more emphasis must therefore be placed on primary prevention, in particular on anti-smoking campaigns, as well as stepping-up research into the etiology of, and novel treatments for other malignant neoplasms, especially colorectal and breast cancers.

BACKGROUND. The selection of clinical trials participants is a critical step in study design, because it affects the generalizability of recommendations made on the basis of trial results and public acceptance of medical research. The authors assessed the heterogeneity of subgroups in cancer treatment and prevention trials and the analysis of subgroups in the evaluation of trial outcomes.METHODS. The authors reviewed published reports (1990-2000) of cancer prevention and treatment trials from 11 journals. They report here on all Phase III cancer treatment and prevention trials that had at least 100 participants and were conducted among adults in the United States. A structured abstract was developed and used to extract data from the 261 published reports. Descriptive summaries of the abstracted data provided the information included in this systematic review.RESULTS. Age and gender of study participants were reported in more than 90% of these trials, whereas fewer than 30% of the trials reported race or ethnicity. Gender was reported as an explicit criterion for participant selection primarily in studies of gender specific malignancies. Race and ethnicity were reported as explicit selection criteria for participant selection for five of the prevention trials and for none of the cancer treatment trials. The 105 treatment trials that reported including both men and women had 42,355 participants, and 38.6% of those participants were women. The 26 prevention trials that reported including both men and women had 73,995 participants, and 34.7% of those participants were women. Fifty-seven treatment trials reported participant ethnic diversity: There were 45,815 participants, with 10.5% African-American participants and with less than 1% Hispanic, Asian, or Native American participants. Seventeen prevention trials reported participant ethnic diversity: There were 91,741 participants, with 5.5% African-American participants, 1.7% Hispanic participants, and less than 1% Asian or Native American participants.CONCLUSIONS. Cancer treatment and prevention trial reports provide scant information about participant race and ethnicity. Such studies use participant selection criteria that do not define diverse subgroups, and few subgroup analyses are conducted. Improvements in the selection, reporting, and analysis of clinical trials participants are needed.

Potential hazards surround us at home, in the workplace, in our cars and even in health care facilities. Given exposure to these hazards, we may want to evaluate the risk that an adverse event will occur or that it will occur at some level of severity. In this article we introduce some concepts

This study was undertaken to identify subgroups of the population susceptible to the effects of ambient air particles. Fixed-site air pollution monitors in Montreal, Quebec, Canada, provided daily mean levels of various measures of particulates and gaseous pollutants. Total sulfates were also measured daily (1986-1993) at a monitoring station 150 km southeast of the city (Sutton, Quebec, Canada). We used coefficient of haze (COH), extinction coefficient, and Sutton sulfates to predict fine particles and sulfates from a fine particles model for days that were missing. We used the universal Quebec medicare system to obtain billings and prescriptions for each Montreal resident who died in the city from 1984 to 1993. These data were then used to define cardiovascular and respiratory conditions that subjects had before death. Using standard Poisson regression time-series analyses, we estimated the association between daily nonaccidental mortality and daily concentrations of particles in the ambient air among persons with cardiovascular and respiratory conditions diagnosed before death. We found no persuasive evidence that daily mortality increased when ambient air particles were elevated for subgroups of persons with chronic upper respiratory diseases, airways disease, cerebrovascular diseases, acute coronary artery disease, and hypertension. However, we found that daily mortality increased linearly as concentrations of particles increased for persons who had acute lower respiratory diseases, chronic coronary artery diseases (especially in the elderly), and congestive heart failure. For this latter set of conditions, the mean percent increase in daily mortality (MPC) for an increase in the COH across its interquartile range (18.5 COH units per 327.8 linear meters), averaged over the day of death and the 2 preceding days, was MPC = 5.09% [95% confidence interval (CI) 2.47-7.79%], MPC = 2.62 (95% CI 0.53-4.75%), and MPC = 4.99 (95% CI 2.44-7.60%), respectively. Adjustments for gaseous pollutants generally attenuated these associations, although the general pattern of increased daily mortality remained. In addition, there appeared to be a stronger association in the summer season. The positive associations found for persons who had acute lower respiratory diseases and congestive heart failure are consistent with some prevailing hypotheses and may also be consistent with recent toxicologic data implicating endothelins. Further epidemiologic studies are required to confirm these findings.

This study was undertaken to determine whether variations in concentrations of particulates in the ambient air of Montreal, Quebec, during the period 1984 to 1993, were associated with daily variations in cause-specific daily mortality. Fixed-site air pollution monitors in Montreal provided daily mean levels of various measures of particles and gaseous pollutants. Total sulfate was also measured daily (1986–1993) at a monitoring station 150 km southeast of the city (Sutton, Quebec). We used coefficient of haze (COH), extinction coefficient, and sulfate from the Sutton station to predict fine particles and sulfate from fine particles for days that were missing. We estimated associations between cause-specific mortality and PM2.5, PM10, predicted fine particles and fine sulfate particles, total suspended particles, coefficient of haze, extinction coefficient, and total sulfate measured at the Sutton station. We selected a set of underlying causes of death, as recorded on the death certificates, as the endpoint and then regressed the logarithm of daily counts of cause-specific mortality on the daily mean levels for the above measures of particulates, after accounting for seasonal and subseasonal fluctuations in the mortality time series, non-Poisson dispersion, weather variables, and gaseous pollutants. We found positive and statistically significant associations between the daily measures of ambient particle mass and sulfate mass and the deaths from respiratory diseases and diabetes. The mean percentage change in daily mortality (MPC), evaluated at the interquartile range for pollutants averaged over the day of death and the preceding 2 days, for deaths from respiratory diseases was MPCCOH=6.90% (95% CI: 3.69–10.21%), MPCPredicted PM2.5= 9.03% (95% CI: 5.83– 12.33%), and MPCSutton sulfate=4.64% (95% CI: 2.46–6.86%). For diabetes, the corresponding estimates were MPCCOH=7.50% (95% CI: 1.96–13.34%), MPCPredicted PM2.5=7.59% (95% CI: 2.36–13.09%), and MPCSutton sulfate=4.48% (95% CI: 1.08–7.99%). Among individuals older than 65 years at time of death, we found consistent associations across our metrics of particles for neoplasms and coronary artery diseases. Associations with sulfate mass were also found among elderly persons who died of cardiovascular diseases and of lung cancer. These associations were consistent with linear relationships. The associations found for respiratory diseases and for cardiovascular diseases, especially in the elderly, are in line with some of the current hypotheses regarding mechanisms by which ambient particles may increase daily mortality. The positive associations found for cancer and for diabetes may be understood through a general hypothesis proposed by Frank and Tankersley, who suggested that persons in failing health may be at higher risk for external insults through the failure of regulating physiological set points. The association with diabetes may be interpreted in light of recent toxicological findings that inhalation of urban particles in animals increases blood pressure and plasmatic levels of endothelins that enhance vasoconstriction and alter electrophysiology. Further research to confirm these findings and to determine whether they are causal is warranted.

The authors investigated the association between daily variations in ozone and cause-specific mortality. Fixed-site air pollution monitors in Montreal, Quebec, provided daily mean levels of ozone, particles, and other gaseous pollutants. Information on the date and underlying cause of death was obtained for residents of Montreal who died in the city between 1984 and 1993. The authors regressed the logarithm of daily counts of cause-specific mortality on mean levels of ozone, after accounting for seasonal and subseasonal fluctuations in the mortality time series, non-Poisson dispersion, and weather variables. The effect of ozone on mortality was generally higher in the warm season and among persons aged 65 years or over. For an increase in the 3-day running mean concentration of ozone of 21.3 microg/m(3), the percentage of increase in daily deaths in the warm season was the following: nonaccidental deaths, 3.3% (95% confidence interval (CI): 1.7, 5.0); cancer, 3.9% (95% CI: 1.0, 6.91); cardiovascular diseases, 2.5% (95% CI: 0.2, 5.0); and respiratory diseases, 6.6% (95% CI: 1.8, 11.8). These results were independent of the effects of other pollutants and were consistent with a log-linear response function.

This study was undertaken in order to shed light on which groups of the general population may be susceptible to the effects of ambient particles. The objectives of the study were (1) to determine whether concentrations of particles in the ambient air of Montreal, Quebec, were associated with daily all-cause and cause-specific mortality in the period 1984 to 1993, and (2) to determine whether groups of the population had higher than average risks of death from exposure to particles. From the network of fixed-site air pollution monitors in Montreal we obtained daily mean levels of various measures of particles, gaseous pollutants, and weather variables measured at Dorval International Airport. We also used measurements of sulfate from an acid rain monitoring station 150 km southeast of the city (Sutton, Quebec). We estimated associations for particulate matter (PM) with an aerodynamic diameter of 10 microns or smaller (PM10), or 2.5 microns or smaller (PM2.5), total suspended particles (TSP), coefficient of haze (COH), an extinction coefficient, and sulfate. Because substantial data for fine particles were missing, we developed a regression model to predict PM2.5 and to predict sulfate from PM2.5. In the main body of the report, we present results for COH, predicted PM2.5, and sulfate. Detailed results for all pollutants are included in Appendices H through O, which are available on request from Health Effects Institute and from the HEI web site at www.healtheffects.org. To address the first objective, we made use of the underlying causes of death among all 140,939 residents of Montreal who died between 1984 and 1993. We regressed the logarithm of daily counts of cause-specific mortality on the daily mean levels for a variety of measures of particles, accounting for seasonal and subseasonal fluctuations in the mortality time series, overdispersion, and weather factors. To address the second objective, we developed algorithms to define conditions that subjects had prior to death, with the focus on cardiopulmonary diseases. These algorithms were based on information retained on the databases of the universal Quebec Health Insurance Plan (QHIP). The databases include records of all procedures (e.g., type of surgery), physician visits, and consultations carried out by all physicians in Quebec. For persons > or = 65 years and for all recipients of social assistance the prescription database contains records of all pharmaceuticals dispensed (type of medication, dose, quantity). For each group of conditions defined, we used the same statistical model that was used in the analyses of all nonaccidental causes of death. In the analyses of cause-specific mortality, we found evidence of associations for all nonaccidental causes of death and specific causes of death--cancer, coronary artery disease, respiratory diseases, and diabetes--that were consistent across most metrics of ambient air particle concentrations, evaluated as the 3-day mean of particle concentrations measured on the day of death (lag 0) and on each of the two days before death (lag 1, lag 2). Associations for all cardiovascular diseases combined were found only with sulfate. As well, we generally found increased daily mortality for persons 65 years of age and over. The results for all nonaccidental causes of death are similar to findings from other studies; the mean percent increase in mortality for a 100 micrograms/m3 increase in daily TSP at lag 0 was 6.7%. In the analyses of the groups defined from the QHIP data, there was little evidence of associations with air pollutants among persons who before death were classified as having acute or chronic upper respiratory diseases, airways diseases, hypertension, acute coronary artery diseases, and cerebrovascular diseases. On the other hand, we found consistent increases across most types of ambient particles for persons who had cancer, acute lower respiratory diseases, any form of cardiovascular disease, chronic coronary artery diseases, and congestive heart failure. As well, we found an association for individuals who did not have any cardiovascular disease, lower respiratory diseases, and cancer. This latter group consisted of persons who had no interactions with the health care system one year before death (12%) and individuals with a wide variety of potentially fatal diseases (52%), including neurological conditions (12%), diabetes (8%), cardiac dysrhythmias (8%), dementia (6%), organic psychotic disorders (6%), and anemias (4%). As statistical power was reduced in the analyses presented above, differences between groups (e.g., < 65 and > or = 65 year age groups) were not usually statistically significant. The association with diabetes has not been reported previously, and this needs to be replicated in other studies. (ABSTRACT TRUNCATED)

Uncertainty in the detection and evaluation of chemical hazards to health leads to challenges when conducting risk assessments. Some of the uncertainty has to do with data, some with incomplete understanding of processes, and some with the most fundamental ways of viewing the questions. True variability--across space, in time, or among individuals--complicates the search for understanding many important aspects of risk. A few statistical and toxicologic tools are available to assess uncertainty. Three methods of classifying uncertainty are briefly discussed. In addition, our disciplinary background may influence how we view and discuss variability and uncertainty. We rarely know as much as we think we do (and not just in risk assessment). Great uncertainty is likely to remain an important part of risk assessment for some decades to come.