A critical survey of all published measurements made so far aimed at retrospective biological dosimetry using fluorescence in situ hybridisation (FISH) techniques on some workers at the Mayak reprocessing plant and on members of the Techa River cohort is given. Each individual has a recorded dose derived from personal monitoring measurements, usually external gamma-rays for Mayak workers or from reconstruction techniques, usually internally derived for the Techa River cohort. From the person's age, which affects the control level, and the stated dose, an expected number of translocations is calculated for each individual and comparisons made to the observed numbers of translocations. From this, an assessment of how well FISH studies can help to validate existing estimates of dose is made. This varies from study to study. Good agreement is generally obtained for the Techa River cohort and lower doses of the Mayak cohort. Rather poorer agreement applies to the more highly exposed Mayak workers. Some of the discrepancy could be because the FISH painting technique was new and was applied to populations before a proper investigation on how to use it for retrospective biological dosimetry had taken place. In addition, too few cells were generally scored per individual so that statistical uncertainties were large.
There is currently no "gold standard" for measuring lifetime sun exposure. Exploration of alternatives to self-reports is important for examining illnesses related to ultraviolet light exposure. Using skin replicas obtained from 184 controls in a breast cancer case-control study (Toronto, Ontario, Canada, 2004-2005), the authors compared self-reported indicators of lifetime sun exposure with two measures of cutaneous microtopography, the Beagley-Gibson system and skin line counts. With the Beagley-Gibson system, significantly increased odds ratios were found for age (odds ratio (OR) = 1.10, 95% confidence interval (CI): 1.05, 1.16), spending 7 days outside per week during the summer (OR = 3.33, 95% CI: 1.48, 7.50), and lifetime number of sunlamp sessions. Significantly decreased odds ratios were found for having darker skin, ever giving birth, and ever using sunlamps. With the skin line count approach, significant positive associations were found for age (OR = 2.31, 95% CI: 1.23, 4.35), age squared, duration of working in outdoor jobs (OR = 0.88, 95% CI: 0.79, 0.98), and average number of outdoor activities per week at ages 20-29 years (OR = 1.05, 95% CI: 1.00, 1.10). While the Beagley-Gibson method was associated with more variables than the skin line count method, both methods require further refinement before graded skin replicas can be recommended as a substitute for self-report measures.
In recent years, there has been escalating concern over the possible association between exposure to pesticides and adverse human health effects by a number of non-governmental organizations, professional and public interest groups. Recognizing the need to document the scientific basis of these concerns as a foundation for initiating a research theme devoted to linkages between exposures to pesticides and human health effects, the Canadian Institutes of Health Research (CIHR) requested a summary of recent research trends that address these linkages. Experts across Canada in the field of pesticide regulation and research were invited to participate in the review. The review summarizes the limitations of past and current studies related to pesticides and human health effects research and makes suggestions for future research priorities and proposed study designs that will improve the assessment of pesticide exposure, the associated health risks, and improved methodology for regulatory decision making.
Adverse health effects of exposure to high levels of air pollutants from biodegradable wastes have been well-studied. However, few investigations have examined the potential effects of chronic exposure to low-to-moderate levels on non-specific health symptoms among residents. Besides, most studies have relied on distances to waste sites to assign exposure status, and have not investigated whether the exposure-symptoms associations are direct or mediated by odor annoyance. In this study, individual-level exposures to a proxy indicator of biodegradable waste pollution (ammonia, NH3) in non-urban residences (n=454) during 2005-2010 were characterized by data from emission-dispersion validated models. Logistic regression and mediating analyses were used to examine associations between exposures and questionnaire-based data on annoyance and non-specific symptoms, after adjusting by person-specific covariates. Strong dose-response associations were found between exposures and annoyance, and between annoyance and symptoms. Associations between exposures and symptoms (nausea, headache, dizziness, difficulty concentrating and unnatural fatigue) were indirect (annoyance-mediated). This study indicates that environmental exposures play an important role in the genesis of non-specific symptoms among residents exposed to low-to-moderate air pollution from biodegradable wastes, although the effects seem to be indirect, relayed through stress-related mechanisms.
Perfluorinated alkylated substances (PFAS) have been extensively used in consumer products and humans are widely exposed to these persistent compounds. A recent study found no association between exposure to perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS) and miscarriage, but no studies have examined adverse effect of the more recently introduced PFASs. We therefore conducted a case-control study within a population-based, prospective cohort during 2010-2012. Newly pregnant women residing in the Municipality of Odense, Denmark were invited to enroll in the Odense Child Cohort at their first antenatal visit before pregnancy week 12. Among a total of 2,874 participating women, 88 suffered a miscarriage and 59 had stored serum samples, of which 56 occurred before gestational week 12. They were compared to a random sample (N=336) of delivering women, who had also donated serum samples before week 12. Using a case-control design, 51 of the women suffering a miscarriage were matched on parity and gestational day of serum sampling with 204 delivering women. In a multiple logistic regression with adjustment for age, BMI, parity and gestational age at serum sampling, women with the highest tertile of exposure to perfluorononanoic acid (PFNA) and perfluorodecanoic acid (PFDA) in pregnancy had odds ratios for miscarriage of 16.5 (95% CI 7.4-36.6-36.5) and 2.67 (1.31-5.44), respectively, as compared to the lowest tertile. In the matched data set, the OR were 37.9 (9.9-145.2) and 3.71 (1.60-8.60), respectively. The association with perfluorohexane sulfonic acid (PFHxS) was in the same direction, but not statistically significant, while no association was found with PFOA and PFOS. Our findings require confirmation due to the possible public health importance, given that all pregnant women are exposed to these widely used compounds.
Growing evidence suggests that air pollution may be a risk factor for breast cancer, but the biological mechanism remains unknown. High mammographic density (MD) is one of the strongest predictors and biomarkers of breast cancer risk, but it has yet to be linked to air pollution. We investigated the association between long-term exposure to traffic-related air pollution and MD in a prospective cohort of women 50 years and older.
For the 4,769 women (3,930 postmenopausal) participants in the Danish Diet, Cancer and Health cohort (1993-1997) who attended mammographic screening in Copenhagen (1993-2001), we used MD assessed at the first screening after cohort entry. MD was defined as mixed/dense or fatty. Traffic-related air pollution at residence was assessed by modeled levels of nitrogen oxides (NOx) and nitrogen dioxide (NO2). The association between mean NOx and NO2 levels since 1971 until cohort baseline (1993-97) and MD was analyzed using logistic regression, adjusting for confounders, and separately by menopause, smoking status, and obesity.
We found inverse, statistically borderline significant associations between long-term exposure to air pollution and having mixed/dense MD in our fully adjusted model (OR; 95% CI: 0.96; 0.93-1.01 per 20 µg/m(3) of NOx and 0.89; 0.80- 0.98 per 10 µg/m(3) of NO2). There was no interaction with menopause, smoking, or obesity.
Traffic-related air pollution exposure does not increase MD, indicating that if air pollution increases breast cancer risk, it is not via MD.
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OBJECTIVES: The Norwegian Mother and Child Cohort Study (MoBa) aims to provide new insights in a broad variety of diseases. The goal of the study is to understand pathways in disease development, and identify preventive measures. Several designs are suitable for studying genetics in complex diseases like asthma and allergy, in MoBa. METHODS: MoBa is a prospective population based cohort of 100 000 pregnancies, following offspring into adulthood. Enrollment started in 1999, and will be completed in 2008. A biobank with samples from the mother, father and child, together with detailed questionnaires from early pregnancy and childhood constitute the basis of the study. When studying complex diseases like asthma, a design with case-parent triads is useful. Parental effects and interactions between maternal and fetal genes can be detected. Stratifying triads by environmental exposure enables assessment of gene-environment interactions. RESULTS: By July 2006, more than 73,000 pregnancies have been included, with nearly 7,000 siblings and 1,300 pairs of twins enrolled. Biological samples are processed and stored at the biobank. The first children are reaching age seven in 2006. CONCLUSION: The MoBa cohort provides an excellent basis for studying genetic, epigenetic and environmental influences on complex diseases.
Schools are supposed to be places where children learn and thrive; not where they, teachers, and other staff get sick. The hazards are many but recognition of those hazards is hard to come by in schools in Canada and the United States. The result can be an uphill fight for school-based organizations and unions. Representatives of four such groups, two each from Canada and the United States, discuss the hazards and their effects. They also have many-often unrecognized-successes and related lessons to share. These include taking comprehensive approaches, looking for broad sweeps and entrees, using building sciences and strategies of solid information, acting with respect and with persistence, including students and parents, going for green cleaners, and using participatory methods. The representatives build on these to discuss what else needs to be done. The ideas are underpinned by the creativity, dedication, and persistence evident in their work to date.
Pesticides have been implicated as likely environmental risk factors for Parkinson disease (PD), but assessment of past exposure to pesticides can be difficult. No prior studies of pesticide exposure and PD used biomarkers of exposure collected before the onset of PD. Our investigation examined the association between prospective serum biomarkers of organochlorine pesticides and PD.
We conducted a nested case-control study within the Finnish Mobile Clinic Health Examination Survey, with serum samples collected during 1968-1972, and analyzed in 2005-2007 for organochlorine pesticides. Incident PD cases were identified through the Social Insurance Institution's nationwide registry and were confirmed by review of medical records (n = 101). Controls (n = 349) were matched for age, sex, municipality, and vital status. Adjusted odds ratios (ORs) of PD were estimated using logistic regression.
Little association emerged with a summary score of the 5 organochlorine pesticides found at high levels, and only increasing dieldrin concentrations trended toward a higher risk of PD (OR per interquartile range [IQR] 1.28, 95% confidence interval [CI] 0.97-1.69, p = 0.08). Because of possible strong confounding by cigarette smoking among smokers, we ran additional analyses restricted to never smokers (n = 68 cases, 183 controls). In these analyses, increasing dieldrin concentrations were associated with increased odds of PD (OR per IQR 1.95, 95% CI 1.26-3.02, p = 0.003). None of the other organochlorine pesticides were associated with PD in these analyses.
These results provide some support for an increased risk of Parkinson disease with exposure to dieldrin, but chance or exposure correlation with other less persistent pesticides could contribute to our findings.
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A systematic review was conducted for the association between animal feeding operations (AFOs) and the health of individuals living near AFOs.
The review was restricted to studies reporting respiratory, gastrointestinal and mental health outcomes in individuals living near AFOs in North America, European Union, United Kingdom, and Scandinavia. From June to September 2008 searches were conducted in PUBMED, CAB, Web-of-Science, and Agricola with no restrictions. Hand searching of narrative reviews was also used. Two reviewers independently evaluated the role of chance, confounding, information, selection and analytic bias on the study outcome. Nine relevant studies were identified. The studies were heterogeneous with respect to outcomes and exposures assessed. Few studies reported an association between surrogate clinical outcomes and AFO proximity. A negative association was reported when odor was the measure of exposure to AFOs and self-reported disease, the measure of outcome. There was evidence of an association between self-reported disease and proximity to AFO in individuals annoyed by AFO odor.
There was inconsistent evidence of a weak association between self-reported disease in people with allergies or familial history of allergies. No consistent dose response relationship between exposure and disease was observable.
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The detection of mutagenic and carcinogenic chlorination by-products in chlorinated drinking water has raised concern in many countries over the potential health effects of long-term exposure to these products. The relation between estimated exposure to historical drinking water mutagenicity and cancer was studied in Finland by using a population-based case-control study comprising 732 bladder cancer cases, 703 kidney cancer cases, and 914 controls. The cases were obtained from the nationwide Finnish Cancer Registry for the years 1991-1992. The controls, frequency matched by age and sex, were randomly selected from the national population registry. Information on past drinking water sources and confounding factors was acquired through a questionnaire. Historical exposure to drinking water mutagenicity was estimated by using information on past residence, past water source, and historical data on water quality and treatment. Odds ratios were calculated for an increase of 3,000 net revertants per liter (net rev/liter) in average exposure from 1950 to 1987, adjusting for age, sex, socioeconomic status, and smoking in logistic regression models. A small, statistically significant, exposure-related excess risk was found for kidney cancer for men (odds ratio = 1.49, 95 percent confidence interval (CI) 1.05-2.13) for 3,000 net rev/liter exposure level. For women, the association remained nonsignificant, with a lower odds ratio of 1.08 (95% CI 0.69-1.68). For bladder cancer, the odds ratio for both men and women was 1.22 (95% CI 0.92-1.62) for 3,000 net rev/liter exposure. However, a higher odds ratio of 2.59 (95% CI 1.13-5.94) for 3,000 net rev/liter exposure was observed for male nonsmokers.
In order to assess the occupational health risk to workers using pesticides, accurate data on exposure (including knowledge of the primary route of exposure) and on absorption are needed. In addition, a well-defined no-effect level (NOEL) derived from suitable animal data must be available. Biological monitoring, urinary metabolite excretion in particular, frequently is used to indicate whether a worker has been exposed. Interpretation of the toxicological significance of the observed urinary metabolite levels is often difficult because the relationship between these levels and toxic dose are generally unknown. Another complication is the apparent lack of correlation between patch data and urinary metabolite data. The usefulness of a metabolite to predict exposure depends on many things, including detailed knowledge of absorption and excretion characteristics of the parent compound and identification of the metabolites. These data, when combined with appropriate toxicology data, permit an analysis of the potential health risks associated with an occupational exposure to toxic chemicals. This paper will correlate data from a number of studies in which the dermal penetration of azinphosmethyl (AM) was measured in rats, rabbits, monkeys and man; and urinary alkyl phosphate metabolites were measured in orchardists exposed to AM. The feasibility of utilizing metabolite excretion to estimate exposure and ultimate risk will be discussed.
Liver and kidney cortex samples were obtained from 89 human autopsies for the determination of metallothionein (MT), cadmium (Cd), zinc (Zn), and copper (Cu). An age-dependent increase of Cd, Zn, and Cd/Zn was observed in the kidney; increases peaked at mid-age and were followed by a decline. Cadmium was present at a low constant level in the liver at all ages. The mean concentrations of Cd and Zn were 18.0 and 40.1 micrograms/g wet weight, respectively, in the kidney, and for the liver the values for Cd and Zn were 2.0 and 79.0 micrograms/g wet weight, respectively. A positive linear relationship was observed between Cd or Zn and MT in the kidney and between Zn and MT in the liver. No other correlation was found between Cu and MT in either organs. Similar values were obtained for MT when estimated by Ag-hem and Cd-hem methods.
We report a further follow-up of a birth cohort of 11 379 workers exposed to chrysotile. The cohort consisted of 10 939 men and 440 women, born 1891-1920, who had worked for at least a month in the mines and mills of Asbestos and Thetford Mines in Quebec. For all subjects, length of service and estimates of accumulated dust exposure were obtained, with a smoking history for the vast majority. Three methods of analysis, two based on the "man-years" methods, the other a "case-and-multiple-controls" approach, gave results consistent with one another and with previous analyses. By the end of 1975, 4463 men and 84 women had died. Among men, the overall excess mortality, 1926-75 was 2% at Asbestos and 10% at Thetford Mines, much the dustier region. The women, mostly employed at Asbestos, had a standardised mortality ratio (SMR) all causes, 1936-75) of 0.90. Analysis of deaths 20 years or more after first employment showed that in men with short service (less than five years) there was no discernible correlation with dust exposure. Among men employed at least 20 years, there were clear excesses in those exposed to the heaviest dust concentrations. Reanalysis in terms of exposure to age 45 showed definite and consistent trends for SMRs for total mortality, for lung cancer, and for pneumoconiosis to be higher the heavier the exposure. The response to increasing dose was effectively linear for lung cancer and for pneumoconiosis. Lung cancer deaths occurred in non-smokers, and showed a greater increase of incidence with increasing exposure than did lung cancer in smokers, but there was insufficient evidence to distinguish between multiplicative and additive risk models. There were no excess deaths from laryngeal cancer, but a clear association with smoking. Ten men and one woman died from pleural mesothelioma. If the only subjects studied had been the 1904 men with at least 20 years' employment in the lower dust concentrations, averaging 6.6 million particles per cubic foot (or about 20 fibres/cc), excess mortality would not have been considered statistically significant, except for pneumoconiosis. The inability of such a large epidemiological survey to detect increased risk at what, today, are considered unacceptable dust concentrations, and the consequent importance of exposure-response models are therefore emphasised.
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BACKGROUND: Blood lead concentrations (B-Pb) were measured in 3 879 Swedish school children during the period 1978-2007. The objective was to study the effect of the proximity to lead sources based on the children's home and school location. METHODS: The children's home address and school location were geocoded and their proximity to a lead smelter and major roads was calculated using geographical information system (GIS) software. All the statistical analyses were carried out using means of generalized log-linear modelling, with natural-logarithm-transformed B-Pb, adjusted for sex, school year, lead-exposing hobby, country of birth and, in the periods 1988-1994 and 1995-2007, parents' smoking habits. RESULTS: The GIS analysis revealed that although the emission from the smelter and children's B-Pb levels had decreased considerably since 1978, proximity to the lead smelter continued to affect levels of B-Pb, even in recent years (geometric mean: near smelter: 22.90 microg/l; far from smelter 19.75 microg/l; p = 0.001). The analysis also revealed that proximity to major roads noticeably affected the children's B-Pb levels during the period 1978-1987 (geometric mean near major roads: 44.26 microg/l; far from roads: 38.32 microg/l; p = 0.056), due to the considerable amount of lead in petrol. This effect was, however, not visible after 1987 due to prohibition of lead in petrol. CONCLUSION: The results show that proximity to the lead smelter still has an impact on the children's B-Pb levels. This is alarming since it could imply that living or working in the vicinity of a former lead source could pose a threat years after reduction of the emission. The analysis also revealed that urban children exposed to lead from traffic were only affected during the early period, when there were considerable amounts of lead in petrol, and that the prohibition of lead in petrol in later years led to reduced levels of lead in the blood of urban children.
Many environmental factors, both indoors and outdoors, can cause or worsen respiratory disease. Although in many cases individuals have little influence over environmental exposures (e.g., weather conditions), there are many (such as environmental tobacco smoke (ETS) and outdoor air pollution) where interventions can improve health. While for environmental exposures such as air pollution, remediation largely devolves to the government, for exposures such as ETS advice to individuals in these settings will confer benefit. Climate change has begun to feature more and more in the context of health but how this may affect pulmonary disease remains debatable. It is possible that heat associated changes in allergen exposures may be more than counterbalanced by potential reductions in cold related exacerbations of diseases such as COPD. An improved assessment of environmental exposures is key in how we approach the effects of the environment on lung disease which would allow better understanding of gene-environment interactions and how remediation might influence population health for the better.
Lifetime risk projections depend greatly on both background lung cancer rates and the selection of the risk model. Since background lung cancer rates differ from subject populations and the time, etiological risk of lifetime lung cancer mortality per unit radon exposure in WLM should be estimated for each subject population and the time of interest. To answer quantitatively how much are the differences among the projected risks for different populations, the Swedish case-control-study-based risk projection model was applied to the Japanese and Swedish populations from 1962 to 1997 as subject populations because of their distinct trends of lung cancer rates. To compare the results with the reference population and authorized risk projection models, U.S. population 1997 and the two risk projection models in BEIR VI report were applied, respectively. Lifetime risk of lung cancer mortality projected for Japanese, Swedish, and U.S. populations in 1997 per radon progeny exposure were estimated to range from 1.50 (0.40-3.19) x 10(-4) WLM(-1) to 9.86 (2.62-20.9) x 10(-4) WLM(-1), which could be compared to the detriment associated with a unit effective dose. Conclusive dose conversion coefficients in this study ranged from 2.05 (0.55-4.37) to 13.5 (3.59-28.6) mSv WLM(-1), and within this range the discrepancy between dosimetric and epidemiological approaches was included.