Skip header and navigation

Refine By

990 records – page 1 of 50.

A critical survey of fish measurements in populations of the southern Urals.

https://arctichealth.org/en/permalink/ahliterature166321
Source
Radiats Biol Radioecol. 2006 Sep-Oct;46(5):619-24
Publication Type
Article
Author
A A Edwards
M. Szluinska
Author Affiliation
Health Protection Agency, Radiation Protection Division, Didcot, Oxfordshire, UK. alan.edwards@hpa-rp.org.uk
Source
Radiats Biol Radioecol. 2006 Sep-Oct;46(5):619-24
Language
English
Publication Type
Article
Keywords
Aged
Chromosome Painting - standards
Data Collection
Dose-Response Relationship, Radiation
Environmental Exposure
Female
Gamma Rays
Humans
In Situ Hybridization, Fluorescence
Male
Middle Aged
Population
Russia
Translocation, Genetic
Water Pollutants, Radioactive - toxicity
Abstract
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.
PubMed ID
17133730 View in PubMed
Less detail

Comparison of self-reported lifetime sun exposure with two methods of cutaneous microtopography.

https://arctichealth.org/en/permalink/ahliterature166563
Source
Am J Epidemiol. 2007 Jan 15;165(2):222-30
Publication Type
Article
Date
Jan-15-2007
Author
Lynn Weiler
Julia A Knight
Reinhold Vieth
Heidi Barnett
Ansely Wong
Author Affiliation
Department of Public Health Sciences, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada.
Source
Am J Epidemiol. 2007 Jan 15;165(2):222-30
Date
Jan-15-2007
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Child
Environmental Exposure
Female
Follow-Up Studies
Humans
Middle Aged
Observer Variation
Ontario
Photomicrography - methods
Replica Techniques
Retrospective Studies
Skin - cytology - radiation effects
Skin Aging - radiation effects
Sunlight
Abstract
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.
PubMed ID
17101707 View in PubMed
Less detail

Addressing the linkage between exposure to pesticides and human health effects--research trends and priorities for research.

https://arctichealth.org/en/permalink/ahliterature166662
Source
J Toxicol Environ Health B Crit Rev. 2006 Nov-Dec;9(6):441-56
Publication Type
Article
Author
L. Ritter
N C I Goushleff
Tye Arbuckle
Donald Cole
Mark Raizenne
Author Affiliation
Canadian Network of Toxicology Centres and Department of Environmental Biology, University of Guelph, Guelph, Ontario, Canada. Iritter@uoguelph.ca
Source
J Toxicol Environ Health B Crit Rev. 2006 Nov-Dec;9(6):441-56
Language
English
Publication Type
Article
Keywords
Canada
Environmental Exposure
Environmental Pollutants - toxicity
Humans
Pesticides - toxicity
Public Health
Public Policy
Research Design
Risk assessment
Abstract
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.
PubMed ID
17090482 View in PubMed
Less detail

Air pollution from biodegradable wastes and non-specific health symptoms among residents: direct or annoyance-mediated associations?

https://arctichealth.org/en/permalink/ahliterature268820
Source
Chemosphere. 2015 Feb;120:371-7
Publication Type
Article
Date
Feb-2015
Author
Victoria Blanes-Vidal
Source
Chemosphere. 2015 Feb;120:371-7
Date
Feb-2015
Language
English
Publication Type
Article
Keywords
Adult
Aged
Air Pollutants - analysis
Ammonia - analysis
Denmark
Environmental Exposure
Female
Health status
Humans
Logistic Models
Male
Middle Aged
Models, Theoretical
Odors - analysis
Self Report
Abstract
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.
PubMed ID
25192839 View in PubMed
Less detail

Association between perfluorinated compound exposure and miscarriage in Danish pregnant women.

https://arctichealth.org/en/permalink/ahliterature269093
Source
PLoS One. 2015;10(4):e0123496
Publication Type
Article
Date
2015
Author
Tina Kold Jensen
Louise Bjørkholt Andersen
Henriette Boye Kyhl
Flemming Nielsen
Henrik Thybo Christesen
Philippe Grandjean
Source
PLoS One. 2015;10(4):e0123496
Date
2015
Language
English
Publication Type
Article
Keywords
Abortion, Spontaneous - chemically induced
Adult
Case-Control Studies
Denmark
Environmental Exposure
Female
Fluorocarbons - toxicity
Humans
Pregnancy
Prospective Studies
Abstract
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.
Notes
Cites: Anal Chem. 2005 Sep 15;77(18):6085-9116159145
Cites: Environ Sci Technol. 2010 Sep 15;44(18):7123-920722423
Cites: Toxicol Sci. 2007 Oct;99(2):366-9417519394
Cites: Environ Health Perspect. 2007 Nov;115(11):1596-60218007991
Cites: J Chromatogr A. 2009 Jan 16;1216(3):385-9319026423
Cites: Am J Epidemiol. 2009 Oct 1;170(7):837-4619692329
Cites: Environ Sci Technol. 2011 Feb 1;45(3):1121-621166449
Cites: Anal Bioanal Chem. 2011 Jun;400(6):1625-3521400077
Cites: Epidemiology. 2012 May;23(3):386-9222370857
Cites: Am J Epidemiol. 2012 Jun 15;175(12):1209-1622517810
Cites: Environ Health Perspect. 2012 Aug;120(8):1201-722450153
Cites: Clin Endocrinol (Oxf). 2013 Sep;79(3):333-4123305099
Cites: Environ Health Perspect. 2013 Oct;121(10):1207-1323838280
Cites: Reproduction. 2014;147(4):443-5324282315
Cites: Epidemiology. 2014 Jul;25(4):505-1224807698
Cites: Toxicol Sci. 2006 Apr;90(2):510-816415327
Cites: Environ Health Perspect. 2010 Aug;118(8):1100-820423814
Cites: Chemosphere. 2014 Dec;116:75-8224792582
PubMed ID
25848775 View in PubMed
Less detail

Long-term exposure to air pollution and mammographic density in the Danish Diet, Cancer and Health cohort.

https://arctichealth.org/en/permalink/ahliterature269405
Source
Environ Health. 2015;14:31
Publication Type
Article
Date
2015
Author
Stephanie Huynh
My von Euler-Chelpin
Ole Raaschou-Nielsen
Ole Hertel
Anne Tjønneland
Elsebeth Lynge
Ilse Vejborg
Zorana J Andersen
Source
Environ Health. 2015;14:31
Date
2015
Language
English
Publication Type
Article
Keywords
Air Pollutants - toxicity
Air Pollution - adverse effects
Breast Neoplasms - chemically induced - epidemiology
Denmark - epidemiology
Environmental Exposure
Environmental monitoring
Female
Humans
Mammary Glands, Human - abnormalities
Middle Aged
Prospective Studies
Risk factors
Vehicle Emissions - toxicity
Abstract
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.
Notes
Cites: Environ Health. 2011;10:6721771295
Cites: Int J Environ Health Res. 2012;22(1):12-2121644128
Cites: Breast Cancer Res Treat. 2012 Feb;132(1):327-3322076479
Cites: Breast Cancer Res. 2011;13(6):22322114898
Cites: J UOEH. 2013 Mar 1;35(1):17-2423475020
Cites: J Natl Cancer Inst. 2013 Apr 17;105(8):515-2523449445
Cites: Cancer Causes Control. 2013 Jul;24(7):1347-5623633026
Cites: PLoS One. 2013;8(12):e8187624349146
Cites: Int J Cancer. 2014 Apr 15;134(8):1871-8824590452
Cites: Environ Int. 2015 Jan;74:240-825454241
Cites: Cancer Causes Control. 2000 Aug;11(7):653-6210977110
Cites: J Med Screen. 2002;9(3):115-912370322
Cites: Cancer Epidemiol Biomarkers Prev. 2003 Oct;12(10):1074-8014578145
Cites: Cancer Epidemiol Biomarkers Prev. 2003 Oct;12(10):1081-614578146
Cites: Cancer Causes Control. 2010 Feb;21(2):301-1119915951
Cites: Environ Health Perspect. 2010 Apr;118(4):511-820064791
Cites: Cancer Epidemiol. 2010 Apr;34(2):142-920197243
Cites: BMJ. 2011;342:d101621363864
Cites: Environ Health Perspect. 2010 Nov;118(11):1578-8320923746
Cites: Environ Health. 2011;10:2221435200
Cites: Scand J Public Health. 2011 Jul;39(7 Suppl):22-521775345
Cites: N Engl J Med. 1982 Oct 21;307(17):1062-57121516
Cites: Arch Environ Health. 1996 Jul-Aug;51(4):255-658757405
Cites: Breast Cancer Res Treat. 1999 Feb;53(3):217-2710369068
Cites: Cancer Causes Control. 2004 Nov;15(9):947-5515577297
Cites: Cancer Epidemiol Biomarkers Prev. 2005 Jan;14(1):53-6015668476
Cites: Cancer Epidemiol Biomarkers Prev. 2006 Jun;15(6):1159-6916775176
Cites: N Engl J Med. 2007 Jan 18;356(3):227-3617229950
Cites: Cancer. 2007 Jun 15;109(12 Suppl):2667-71117503436
Cites: J Natl Cancer Inst. 2007 Aug 1;99(15):1178-8717652278
Cites: Cancer Causes Control. 2007 Nov;18(9):947-5517632764
Cites: Scand J Public Health. 2007;35(4):432-4117786808
Cites: Breast Cancer Res. 2007;9(5):R7317963507
Cites: Curr Med Res Opin. 2008 Feb;24(2):365-818096111
Cites: Cancer Causes Control. 2008 May;19(4):43518066671
Cites: Br J Cancer. 2009 Apr 7;100(7):1205-819293800
Cites: Am J Epidemiol. 2009 Dec 15;170(12):1571-819910376
PubMed ID
25879829 View in PubMed
Less detail

Genetics and gene-environment interactions in atopic diseases. The Norwegian Mother and Child Cohort Study.

https://arctichealth.org/en/permalink/ahliterature87519
Source
Hum Hered. 2008;65(4):195-8
Publication Type
Article
Date
2008
Author
Håberg Siri E
Nafstad Per
Nystad Wenche
Magnus Per
Author Affiliation
Division of Epidemiology, Norwegian Institute of Public Health, Oslo, Norway. siri.haberg@fhi.no
Source
Hum Hered. 2008;65(4):195-8
Date
2008
Language
English
Publication Type
Article
Keywords
Child
Child, Preschool
Cohort Studies
Environmental Exposure
Fathers
Female
Genetic Predisposition to Disease
Humans
Hypersensitivity - epidemiology - etiology
Infant
Male
Mothers
Norway - epidemiology
Pregnancy
Questionnaires
Risk factors
Abstract
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.
PubMed ID
18073489 View in PubMed
Less detail

"We can't give up. It's too important." Health and safety stories from Canadian and U.S. schools.

https://arctichealth.org/en/permalink/ahliterature144533
Source
New Solut. 2010;20(1):81-93
Publication Type
Article
Date
2010
Author
Dorothy Wigmore
Author Affiliation
dorothyw@web.ca
Source
New Solut. 2010;20(1):81-93
Date
2010
Language
English
Publication Type
Article
Keywords
Canada
Community-Based Participatory Research
Environment
Environmental Exposure
Environmental health
Health status
Humans
Occupational Exposure
Safety
Schools - organization & administration
United States
Abstract
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.
PubMed ID
20359993 View in PubMed
Less detail

Persistent organochlorine pesticides in serum and risk of Parkinson disease.

https://arctichealth.org/en/permalink/ahliterature144595
Source
Neurology. 2010 Mar 30;74(13):1055-61
Publication Type
Article
Date
Mar-30-2010
Author
M G Weisskopf
P. Knekt
E J O'Reilly
J. Lyytinen
A. Reunanen
F. Laden
L. Altshul
A. Ascherio
Author Affiliation
Harvard School of Public Health, Department of Environmental Health, Landmark Center, Boston, MA 02215, USA. mweissko@hsph.harvard.edu
Source
Neurology. 2010 Mar 30;74(13):1055-61
Date
Mar-30-2010
Language
English
Publication Type
Article
Keywords
Adult
Aged
Case-Control Studies
Dieldrin - blood
Environmental Exposure
Female
Finland - epidemiology
Humans
Hydrocarbons, Chlorinated - blood
Logistic Models
Male
Middle Aged
Odds Ratio
Parkinson Disease - blood - epidemiology
Pesticides - blood
Registries
Risk factors
Smoking
Young Adult
Abstract
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.
Notes
Cites: Mov Disord. 1999 Nov;14(6):928-3910584666
Cites: Ann Neurol. 2009 Oct;66(4):494-50419847896
Cites: J Expo Anal Environ Epidemiol. 2000 Nov-Dec;10(6 Pt 2):743-5411138666
Cites: FEBS Lett. 2001 Jul 6;500(3):105-811445065
Cites: Neurology. 2001 Oct 23;57(8):1497-911673599
Cites: J Neurol Neurosurg Psychiatry. 2002 Nov;73(5):529-3412397145
Cites: Arch Environ Health. 2003 Jan;58(1):30-612747516
Cites: Am J Epidemiol. 1986 Oct;124(4):693-7013752063
Cites: Am J Epidemiol. 1988 Jan;127(1):28-413276161
Cites: Arch Environ Contam Toxicol. 1989 Jul-Aug;18(4):495-5002505694
Cites: Ann Neurol. 1994 Jul;36(1):100-37517654
Cites: Neurology. 1996 May;46(5):1275-848628466
Cites: Exp Neurol. 1998 Apr;150(2):339-429527905
Cites: Arch Neurol. 1999 Jan;56(1):33-99923759
Cites: JAMA. 1999 Jan 27;281(4):341-69929087
Cites: Int J Circumpolar Health. 2004;63 Suppl 2:366-815736686
Cites: Neurotoxicology. 2005 Aug;26(4):701-1916112328
Cites: Environ Health Perspect. 2005 Dec;113(12):1712-616330352
Cites: Environ Health Perspect. 2006 Feb;114(2):156-6416451848
Cites: Am J Epidemiol. 2007 Feb 15;165(4):364-7417116648
Cites: Exp Neurol. 2007 Apr;204(2):619-3017291500
Cites: J Neurol Sci. 2007 Nov 15;262(1-2):37-4417673256
Cites: J Neurol Neurosurg Psychiatry. 2008 Apr;79(4):368-7618344392
Cites: BMC Neurol. 2008;8:618373838
Cites: Trends Pharmacol Sci. 2008 Jun;29(6):322-918453001
Cites: Neurotoxicology. 2008 Jul;29(4):584-9018455239
Cites: Neurotoxicology. 2008 Jul;29(4):682-9018533268
Cites: Am J Epidemiol. 2009 Apr 15;169(8):919-2619270050
Cites: Arch Neurol. 2009 Jul;66(7):870-519597089
Cites: Arch Neurol. 2009 Sep;66(9):1106-1319752299
Cites: J Toxicol Environ Health A. 2000 Feb 25;59(4):229-3410706031
PubMed ID
20350979 View in PubMed
Less detail

The association between proximity to animal feeding operations and community health: a systematic review.

https://arctichealth.org/en/permalink/ahliterature144912
Source
PLoS One. 2010;5(3):e9530
Publication Type
Article
Date
2010
Author
Annette M O'Connor
Brent Auvermann
Danelle Bickett-Weddle
Steve Kirkhorn
Jan M Sargeant
Alejandro Ramirez
Susanna G Von Essen
Author Affiliation
Department of Veterinary Diagnostic and Production Animal Medicine, College of Veterinary Medicine, Iowa State University, Ames, Iowa, United States of America. oconnor@iastate.edu
Source
PLoS One. 2010;5(3):e9530
Date
2010
Language
English
Publication Type
Article
Keywords
Animal Feed
Animal Husbandry
Animals
Environmental Exposure
European Union
Gastrointestinal Diseases - epidemiology - etiology
Great Britain
Humans
Inhalation Exposure - adverse effects
Mental health
North America
Respiratory Tract Diseases - epidemiology - etiology
Scandinavia
Abstract
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.
Notes
Cites: Environ Health Perspect. 2000 Aug;108 Suppl 4:705-1210931789
Cites: Environ Health Perspect. 2000 Mar;108(3):233-810706529
Cites: Environ Health Perspect. 2000 Aug;108(8):685-9910964788
Cites: Emerg Infect Dis. 2002 Mar;8(3):252-711927021
Cites: Environ Health Perspect. 2002 May;110(5):437-4412003746
Cites: Minn Med. 2002 Oct;85(10):38-4312416314
Cites: Epidemiology. 2004 Jan;15(1):36-4514712145
Cites: Environ Sci Technol. 2003 Dec 15;37(24):5471-814717153
Cites: Epidemiol Infect. 2004 Apr;132(2):317-2515061507
Cites: Epidemiol Infect. 2004 Jun;132(3):495-50515188718
Cites: Ann Agric Environ Med. 2004;11(1):59-6215236499
Cites: Am J Ind Med. 2004 Oct;46(4):345-815376225
Cites: Epidemiol Infect. 2004 Oct;132(5):967-7615473161
Cites: West J Med. 1982 Nov;137(5):436-77179963
Cites: Int J Food Microbiol. 1991 Jul;13(3):231-71892741
Cites: Arch Environ Health. 1992 Jan-Feb;47(1):76-871540008
Cites: Chest. 1992 Mar;101(3):767-741541145
Cites: Am J Ind Med. 1995 Mar;27(3):405-187747746
Cites: Environ Health Perspect. 1995 Oct;103 Suppl 7:3-48593871
Cites: J Eval Clin Pract. 1995 Nov;1(2):127-309238567
Cites: Am J Respir Crit Care Med. 1998 Jan;157(1):15-89445272
Cites: Nutr Rev. 1998 Apr;56(4 Pt 1):95-1059584494
Cites: Annu Rev Public Health. 1998;19:173-2029611617
Cites: J Anim Sci. 1998 May;76(5):1343-559621940
Cites: J Anim Sci. 1998 Oct;76(10):2641-89814905
Cites: Clin Exp Allergy. 1999 Jan;29(1):28-3410051699
Cites: Epidemiol Infect. 1999 Apr;122(2):193-20010355782
Cites: J Clin Epidemiol. 2004 Nov;57(11):1147-5215567630
Cites: Ann Agric Environ Med. 2004;11(2):163-7315627320
Cites: Environ Health Perspect. 2005 Feb;113(2):137-4215687049
Cites: Environ Health Perspect. 2005 May;113(5):567-7615866765
Cites: Arch Environ Health. 2004 Feb;59(2):101-816075904
Cites: Epidemiol Infect. 2005 Dec;133(6):1033-4116274499
Cites: Pneumologie. 2005 Dec;59(12):897-90016379061
Cites: Environ Health Perspect. 2006 Apr;114(4):591-616581551
Cites: J Agromedicine. 2005;10(4):55-6416702123
Cites: Chest. 2006 Jun;129(6):1486-9116778265
Cites: Pediatrics. 2006 Jul;118(1):e66-7516818539
Cites: Gesundheitswesen. 2006 Aug-Sep;68(8-9):575-8417039438
Cites: Environ Health Perspect. 2007 Feb;115(2):296-717384781
Cites: Environ Health Perspect. 2007 Feb;115(2):298-30217384782
Cites: Environ Health Perspect. 2007 Feb;115(2):308-1217384784
Cites: Environ Health Perspect. 2007 Feb;115(2):313-617384785
Cites: Environ Health Perspect. 2007 Feb;115(2):317-2017384786
Cites: Epidemiology. 2007 May;18(3):300-817435437
Cites: Environ Res. 2007 Nov;105(3):400-817493608
Cites: Emerg Infect Dis. 2007 Dec;13(12):1834-918258032
Cites: New Solut. 2008;18(2):193-20518511396
Cites: Am J Public Health. 2008 Aug;98(8):1390-718556620
Cites: Prev Med. 2009 Jan;48(1):45-5319026676
Cites: Methods Mol Biol. 2009;473:1-1719160729
Cites: N Engl J Med. 2002 Sep 19;347(12):869-7712239255
Cites: J Agromedicine. 2006;11(3-4):15-2419274894
Cites: Epidemiol Infect. 2009 Jun;137(6):810-2018947443
Cites: BMC Health Serv Res. 2008;8:27019102752
Cites: AIDS Behav. 2009 Oct;13(5):949-6819330443
Cites: Lancet. 1999 Nov 27;354(9193):1896-90010584742
Cites: Environ Health Perspect. 2000 Oct;108(10):997-100211049823
PubMed ID
20224825 View in PubMed
Less detail

Drinking water mutagenicity and urinary tract cancers: a population-based case-control study in Finland.

https://arctichealth.org/en/permalink/ahliterature204251
Source
Am J Epidemiol. 1998 Oct 1;148(7):704-12
Publication Type
Article
Date
Oct-1-1998
Author
M. Koivusalo
T. Hakulinen
T. Vartiainen
E. Pukkala
J J Jaakkola
J. Tuomisto
Author Affiliation
Finnish Cancer Registry, Helsinki.
Source
Am J Epidemiol. 1998 Oct 1;148(7):704-12
Date
Oct-1-1998
Language
English
Publication Type
Article
Keywords
Adult
Aged
Case-Control Studies
Chlorine - adverse effects
Environmental Exposure
Female
Finland - epidemiology
Humans
Male
Middle Aged
Mutagenicity Tests
Odds Ratio
Prevalence
Risk factors
Sex Factors
Urologic Neoplasms - epidemiology - etiology - genetics
Water Supply - analysis - standards
Abstract
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.
PubMed ID
9778177 View in PubMed
Less detail

[Status of the deciduous teeth in young children with sociobiological risk factors in their anamnesis].

https://arctichealth.org/en/permalink/ahliterature236416
Source
Stomatologiia (Mosk). 1986 Nov-Dec;65(6):16-8
Publication Type
Article

The use of biological monitoring in the estimation of exposure during the application of pesticides.

https://arctichealth.org/en/permalink/ahliterature236517
Source
Toxicol Lett. 1986 Oct;33(1-3):127-36
Publication Type
Article
Date
Oct-1986
Author
C A Franklin
N I Muir
R P Moody
Source
Toxicol Lett. 1986 Oct;33(1-3):127-36
Date
Oct-1986
Language
English
Publication Type
Article
Keywords
Agriculture
Animals
Canada
Chromatography, High Pressure Liquid
Environmental Exposure
Haplorhini
Humans
Male
Organophosphate Poisoning
Organothiophosphates - metabolism - urine
Organothiophosphorus Compounds - metabolism
Protective Clothing
Rabbits
Rats
Skin Absorption
Skin Tests
Abstract
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.
PubMed ID
3095958 View in PubMed
Less detail

Metallothionein levels in liver and kidney of Canadians--a potential indicator of environmental exposure to cadmium.

https://arctichealth.org/en/permalink/ahliterature236571
Source
Arch Environ Health. 1986 Sep-Oct;41(5):319-23
Publication Type
Article
Author
J. Chung
N O Nartey
M G Cherian
Source
Arch Environ Health. 1986 Sep-Oct;41(5):319-23
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Cadmium - analysis
Canada
Child
Copper - analysis
Environmental Exposure
Female
Fetus - analysis
Humans
Kidney - analysis
Liver - analysis
Male
Metallothionein - analysis
Middle Aged
Spectrophotometry, Atomic
Zinc - analysis
Abstract
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.
PubMed ID
3800437 View in PubMed
Less detail

Environmental lead and young children.

https://arctichealth.org/en/permalink/ahliterature245686
Source
Can Med Assoc J. 1980 Jun 21;122(12):1347-8
Publication Type
Article
Date
Jun-21-1980
Author
C J Mackenzie
Source
Can Med Assoc J. 1980 Jun 21;122(12):1347-8
Date
Jun-21-1980
Language
English
Publication Type
Article
Keywords
Canada
Child, Preschool
Environmental Exposure
Humans
Lead Poisoning - epidemiology
United States
Notes
Cites: N Engl J Med. 1979 Mar 29;300(13):689-95763299
Cites: N Engl J Med. 1979 Jul 19;301(3):161449963
Cites: JAMA. 1979 Aug 24-31;242(8):739-41459063
Cites: Can Med Assoc J. 1979 Dec 8;121(11):1474-8519574
Cites: Lancet. 1970 Oct 3;2(7675):695-84195933
Cites: Arch Environ Health. 1974 Apr;28(4):195-74131149
Cites: Toxicol Appl Pharmacol. 1975 Jun;32(3):628-371154418
Cites: N Engl J Med. 1975 Jan 16;292(3):123-91196336
Cites: Am Ind Hyg Assoc J. 1976 Sep;37(9):541-51008036
Cites: J Air Pollut Control Assoc. 1977 Aug;27(8):763-7886085
Cites: Brain Res. 1978 Jun 16;148(2):451-67656942
Cites: Environ Res. 1978 Apr;15(2):290-308668659
PubMed ID
7260739 View in PubMed
Less detail

Dust exposure and mortality in chrysotile mining, 1910-75.

https://arctichealth.org/en/permalink/ahliterature246109
Source
Br J Ind Med. 1980 Feb;37(1):11-24
Publication Type
Article
Date
Feb-1980
Author
J C McDonald
F D Liddell
G W Gibbs
G E Eyssen
A D McDonald
Source
Br J Ind Med. 1980 Feb;37(1):11-24
Date
Feb-1980
Language
English
Publication Type
Article
Keywords
Accidents
Aged
Asbestos - adverse effects
Asbestosis - mortality
Cerebrovascular Disorders - mortality
Dust
Employment
Environmental Exposure
Female
Follow-Up Studies
Heart Diseases - mortality
Humans
Lung Neoplasms - mortality
Male
Middle Aged
Mining
Neoplasms - mortality
Occupational Diseases - mortality
Quebec
Respiration Disorders - mortality
Smoking - complications
Time Factors
Abstract
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.
Notes
Cites: Biometrics. 1969 Jun;25(2):339-555794104
Cites: Arch Environ Health. 1971 Jun;22(6):677-865574010
Cites: Arch Environ Health. 1972 Mar;24(3):189-975059627
Cites: Arch Environ Health. 1974 Feb;28(2):61-84809914
Cites: Arch Environ Health. 1974 Feb;28(2):69-714809915
Cites: Arch Environ Health. 1975 May;30(5):266-71130842
Cites: Br J Prev Soc Med. 1976 Dec;30(4):225-301009272
Cites: Int J Cancer. 1977 Sep 15;20(3):323-31903186
Cites: Prev Med. 1977 Sep;6(3):426-42333420
Cites: J Occup Med. 1977 Nov;19(11):737-40915568
Cites: Lancet. 1978 Mar 4;1(8062):484-976030
Cites: Br J Ind Med. 1964 Oct;21:304-714253230
PubMed ID
7370189 View in PubMed
Less detail

Geographical patterns in blood lead in relation to industrial emissions and traffic in Swedish children, 1978-2007.

https://arctichealth.org/en/permalink/ahliterature95183
Source
BMC Public Health. 2009;9:225
Publication Type
Article
Date
2009
Author
Stroh Emilie
Lundh Thomas
Oudin Anna
Skerfving Staffan
Strömberg Ulf
Author Affiliation
Department of Laboratory Medicine, Lund University, Lund, Sweden. emilie.stroh@med.lu.se
Source
BMC Public Health. 2009;9:225
Date
2009
Language
English
Publication Type
Article
Keywords
Adolescent
Air Pollutants
Child
Environmental Exposure
Geographic Information Systems
Humans
Industrial Waste
Lead - blood
Sweden - epidemiology
Vehicle Emissions
Abstract
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.
PubMed ID
19591669 View in PubMed
Less detail

The non-occupational environment and the lung: opportunities for intervention.

https://arctichealth.org/en/permalink/ahliterature95584
Source
Chron Respir Dis. 2007;4(4):227-36
Publication Type
Article
Date
2007
Author
Kurmi O P
Ayres J G
Author Affiliation
Department of Environmental and Occupational Medicine, Liberty Safe Work Research Centre, University of Aberdeen, Aberdeen, UK.
Source
Chron Respir Dis. 2007;4(4):227-36
Date
2007
Language
English
Publication Type
Article
Keywords
Air Pollutants - pharmacology
Air Pollution, Indoor - adverse effects
Asthma - epidemiology
Climate
Environmental Exposure
Humans
Lung
Weather
Abstract
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.
PubMed ID
18029436 View in PubMed
Less detail

Lifetime risk of lung cancer due to radon exposure projected to Japanese and Swedish populations.

https://arctichealth.org/en/permalink/ahliterature19764
Source
Health Phys. 2001 Jun;80(6):552-62
Publication Type
Article
Date
Jun-2001
Author
M. Doi
Y. Nakamura
T. Sakashita
N. Ogiu
F. Lagarde
R. Falk
Author Affiliation
Environmental and Toxicological Sciences, Research Group, National Institute of Radiological Sciences, Inage, Chiba, Japan. masa_doi@nirs.go.jp
Source
Health Phys. 2001 Jun;80(6):552-62
Date
Jun-2001
Language
English
Publication Type
Article
Keywords
Environmental Exposure
Female
Humans
Japan
Lung Neoplasms - etiology - mortality
Male
Models, Theoretical
Neoplasms, Radiation-Induced - mortality
Radon - adverse effects
Risk assessment
Sweden
United States
Abstract
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.
PubMed ID
11388724 View in PubMed
Less detail

990 records – page 1 of 50.