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Accumulation of Major Life Events in Childhood and Adult Life and Risk of Type 2 Diabetes Mellitus.

https://arctichealth.org/en/permalink/ahliterature273707
Source
PLoS One. 2015;10(9):e0138654
Publication Type
Article
Date
2015
Author
Jolene Masters Pedersen
Naja Hulvej Rod
Ingelise Andersen
Theis Lange
Gry Poulsen
Eva Prescott
Rikke Lund
Source
PLoS One. 2015;10(9):e0138654
Date
2015
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Denmark - epidemiology
Diabetes Mellitus, Type 2 - epidemiology - etiology
Female
Follow-Up Studies
Humans
Life Change Events
Logistic Models
Male
Middle Aged
Multivariate Analysis
Risk Assessment - methods - statistics & numerical data
Risk factors
Stress, Psychological - complications
Surveys and Questionnaires
Time Factors
Young Adult
Abstract
The aim of the study was to estimate the effect of the accumulation of major life events (MLE) in childhood and adulthood, in both the private and working domains, on risk of type 2 diabetes mellitus (T2DM). Furthermore, we aimed to test the possible interaction between childhood and adult MLE and to investigate modification of these associations by educational attainment.
The study was based on 4,761 participants from the Copenhagen City Heart Study free of diabetes at baseline and followed for 10 years. MLE were categorized as 0, 1, 2, 3 or more events. Multivariate logistic regression models adjusted for age, sex, education and family history of diabetes were used to estimate the association between MLE and T2DM.
In childhood, experiencing 3 or more MLE was associated with a 69% higher risk of developing T2DM (Odds Ratio (OR) 1.69; 95% Confidence Interval (CI) 1.60, 3.27). The accumulation of MLE in adult private (p-trend = 0.016) and work life (p-trend = 0.049) was associated with risk of T2DM in a dose response manner. There was no evidence that experiencing MLE in both childhood and adult life was more strongly associated with T2DM than experiencing events at only one time point. There was some evidence that being simultaneously exposed to childhood MLE and short education (OR 2.28; 95% C.I. 1.45, 3.59) and work MLE and short education (OR 2.86; 95% C.I. 1.62, 5.03) was associated with higher risk of T2DM, as the joint effects were greater than the sum of their individual effects.
Findings from this study suggest that the accumulation of MLE in childhood, private adult life and work life, respectively, are risk factors for developing T2DM.
Notes
Cites: Psychol Med. 2004 Apr;34(3):509-2015259836
Cites: Psychoneuroendocrinology. 2005 Jan;30(1):1-1015358437
Cites: Acta Psychiatr Scand Suppl. 2003;(418):61-612956817
Cites: Arch Intern Med. 2004 Sep 27;164(17):1873-8015451762
Cites: J Psychosom Res. 1967 Aug;11(2):213-86059863
Cites: Soc Sci Med. 1987;25(6):567-783317881
Cites: J Health Soc Behav. 1990 Jun;31(2):162-722102495
Cites: Epidemiology. 1992 Sep;3(5):452-61391139
Cites: J Clin Epidemiol. 1996 Dec;49(12):1407-178970491
Cites: Epidemiology. 1999 Jan;10(1):37-489888278
Cites: Ann N Y Acad Sci. 2004 Dec;1032:276-815677427
Cites: J Epidemiol Community Health. 2006 Jan;60(1):7-1216361448
Cites: Ann Intern Med. 2007 Oct 16;147(8):W163-9417938389
Cites: Pediatrics. 2008 May;121(5):e1240-918450866
Cites: Diabet Med. 2008 Jul;25(7):834-4218513304
Cites: Diabet Med. 2008 Oct;25(10):1211-719046200
Cites: Ann Med. 2009;41(1):66-7218720095
Cites: J Intern Med. 2009 Nov;266(5):467-7519570055
Cites: Discov Med. 2010 Feb;9(45):112-820193636
Cites: Endocrinol Metab Clin North Am. 2010 Sep;39(3):481-9720723815
Cites: Am J Prev Med. 2010 Dec;39(6):529-3621084073
Cites: Int J Epidemiol. 2011 Aug;40(4):904-1321441553
Cites: Curr Psychiatry Rep. 2012 Feb;14(1):8-1422094982
Cites: Physiol Behav. 2012 Apr 12;106(1):29-3921888923
Cites: Gen Hosp Psychiatry. 2014 Jan-Feb;36(1):26-3224183489
Cites: Eur J Public Health. 2014 Feb;24(1):57-6223397581
Cites: Diabetes Care. 2000 Feb;23(2):197-20110868831
Cites: Scand Cardiovasc J. 2001 Jul;35(3):172-711515689
Cites: J Aging Health. 2002 Nov;14(4):467-9412392001
PubMed ID
26394040 View in PubMed
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Alcohol consumption and pancreatitis mortality in Russia.

https://arctichealth.org/en/permalink/ahliterature262739
Source
JOP. 2014 Jul;15(4):365-70
Publication Type
Article
Date
Jul-2014
Author
Yury E Razvodovsky
Source
JOP. 2014 Jul;15(4):365-70
Date
Jul-2014
Language
English
Publication Type
Article
Keywords
Alcohol Drinking - adverse effects
Female
Humans
Male
Pancreatitis - etiology - mortality
Risk Assessment - methods - statistics & numerical data
Risk factors
Russia - epidemiology
Survival Rate - trends
Time Factors
Abstract
Pancreatitis is a major public health problem with high associated economic costs. The incidence of pancreatitis has increased in many European countries in recent decade. Accumulated research and empirical evidence suggests that excessive alcohol consumption is a major risk factor for both acute and chronic pancreatitis.
The aim of this study was to examine the aggregate-level relation between the alcohol consumption and pancreatitis mortality rates in Russia.
Age-standardized sex-specific male and female pancreatitis mortality data for the period 1970-2005 and data on overall alcohol consumption were analyzed by means ARIMA (autoregressive integrated moving average) time series analysis.
Alcohol consumption was significantly associated with both male and female pancreatitis mortality rates: a 1 liter increase in overall alcohol consumption would result in a 7.0% increase in the male pancreatitis mortality rate and in 2.3% increase in the female mortality rate. The results of the analysis suggest that 63.1% of all male pancreatitis deaths and 26.8% female deaths in Russia could be attributed to alcohol. Conclusions The outcomes of this study provide indirect support for the hypothesis that unfavorable mixture of higher overall level of alcohol consumption and binge drinking pattern is an important contributor to the pancreatitis mortality rate in Russian Federation.
PubMed ID
25076345 View in PubMed
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Assessing the effect of treatment duration on the association between anti-diabetic medication and cancer risk.

https://arctichealth.org/en/permalink/ahliterature265055
Source
PLoS One. 2014;9(11):e113162
Publication Type
Article
Date
2014
Author
Anna But
Haining Wang
Satu Männistö
Eero Pukkala
Jari Haukka
Source
PLoS One. 2014;9(11):e113162
Date
2014
Language
English
Publication Type
Article
Keywords
Adult
Aged
Body mass index
Cohort Studies
Cross-Sectional Studies
Diabetes Mellitus, Type 1 - drug therapy
Diabetes Mellitus, Type 2 - drug therapy
Female
Finland - epidemiology
Follow-Up Studies
Health Surveys - methods - statistics & numerical data
Humans
Hypoglycemic agents - therapeutic use
Incidence
Male
Middle Aged
Neoplasms - epidemiology
Registries - statistics & numerical data
Risk Assessment - methods - statistics & numerical data
Risk factors
Smoking
Time Factors
Abstract
Most studies that have evaluated the association between anti-diabetic medication and cancer risk have suffered from methodological drawbacks. To avoid time-related biases, we evaluated the effect of treatment duration on the cancer risk among naive users of anti-diabetic medication as compared to non-users. In addition, we addressed the influence of common risk factors such as smoking and BMI. The study population comprised 23,394 participants of FINRISK surveys. Data on cancer and anti-diabetic medication were linked with the study cohorts. We applied Lexis tabulation to the data and analyzed split records by using Poisson regression. Changes in cancer incidence in relation to treatment duration were examined by modeling the rate ratio (RR). After a median follow-up of 9 years, 53 cancer cases among users of anti-diabetic medication and 1,028 among non-users were diagnosed. No significant difference in cancer risk between users and non-users was observed after adjustment. The RR for all medication regardless of its duration was 1.01 [95% CI 0.75-1.33], and 1.37 [0.94-1.94] for period of 1-4 years. The results were similar for metformin, sulfonylurea, and insulin. This study demonstrates that evaluation of the variation in cancer risk in relation to treatment duration is of particular importance for enhancing the accuracy of conclusions on the link between exposure to anti-diabetic medication and cancer risk.
Notes
Cites: Adv Exp Med Biol. 2012;771:229-3923393682
Cites: Cancer Prev Res (Phila). 2014 Sep;7(9):867-8524985407
Cites: Am J Med. 2013 Sep;126(9 Suppl 1):S10-2023953074
Cites: Endocr Pract. 2013 Jul-Aug;19(4):675-9323978590
Cites: Diabetes Care. 2013 Oct;36(10):3070-523990517
Cites: Diabetes Care. 2013 Dec;36(12):3953-6024170756
Cites: Eur J Cancer Prev. 2014 Mar;23(2):134-4023962874
Cites: Lancet Diabetes Endocrinol. 2013 Oct;1(2):132-924622319
Cites: Int J Epidemiol. 2001 Oct;30 Suppl 1:S35-4011759849
Cites: Diabetes Care. 2003 Jan;26(1):61-912502659
Cites: Diabetes Care. 2004 May;27(5):1047-5315111519
Cites: Am J Med. 1992 Jul 15;93(1A):13S-17S1496998
Cites: Acta Oncol. 1994;33(4):365-98018367
Cites: Diabetologia. 2010 Sep;53(9):1867-7620490448
Cites: Diabet Med. 2011 May;28(5):583-921294766
Cites: Diabetologia. 2011 Sep;54(9):2263-7121748485
Cites: Diabetologia. 2012 Mar;55(3):654-6522127412
Cites: APMIS Suppl. 1997;76:141-69462826
Cites: BMJ. 2005 Sep 24;331(7518):65616179700
Cites: Lancet. 2006 May 27;367(9524):1747-5716731270
Cites: JAMA. 2007 Dec 12;298(22):2654-6418073361
Cites: Lancet. 2009 Jun 27;373(9682):2215-2119515410
Cites: Int J Cancer. 2010 Feb 1;126(3):692-70219645011
Cites: Endocr Pract. 2013 Mar-Apr;19(2):327-3623598536
Cites: Am J Med. 2012 Mar;125(3):302.e1-722340932
Cites: Diabetologia. 2012 Apr;55(4):948-5822120574
Cites: Diabetologia. 2012 Jun;55(6):1607-1822476947
Cites: Diabetologia. 2012 Jun;55(6):1619-3222476948
Cites: Diabetes Care. 2012 Dec;35(12):2665-7323173135
Cites: Eur J Cancer. 2014 Aug;50(12):2119-2524930060
Cites: Int J Epidemiol. 2010 Apr;39(2):504-1819959603
PubMed ID
25419576 View in PubMed
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[Assessment of carcinogenic risks to workers of the main enterprises of the Irkutsk region].

https://arctichealth.org/en/permalink/ahliterature290289
Source
Gig Sanit. 2016; 95(12):1163-7
Publication Type
Journal Article
Author
N V Efimova
V S Rukavishnikov
V A Pankov
A N Perezhogin
S F Shayakhmetov
N M Meshchakova
L G Lisetskaya
Source
Gig Sanit. 2016; 95(12):1163-7
Language
Russian
Publication Type
Journal Article
Keywords
Air Pollutants, Occupational - analysis - toxicity
Carcinogenesis - chemically induced
Carcinogens, Environmental - analysis - toxicity
Chromium - analysis - toxicity
Formaldehyde - analysis - toxicity
Humans
Manufacturing Industry - methods - standards
Occupational Exposure - adverse effects - analysis - prevention & control
Risk Assessment - methods - statistics & numerical data
Risk factors
Siberia - epidemiology
Time
Vinyl Chloride - analysis - toxicity
Abstract
The purpose of research is the assessment of the individual cancer risk (ICR) for workers of the basic occupations in key branches of industry of the Irkutsk region. There was executed the calculation of ICR levels for workers of the basic occupations of the aircraft industry, aluminum smelters and vinyl chloride production plants. The estimation of the exposure for workers was carried out according to long-term time-weighted average concentrations in the air of the working area, for the population - on annual average concentrations in the ambient air. To assess the risk that is not associated with the profession, the dose was calculated for the period of life (70 years). When calculating the toxicant doses in the working area there were used the “standard” indices ofpulmonary ventilation for adults, body weight, the work experience in the contact with carcinogens of 30 years, the number of days in the contact of 240, the duration of the working time 8 or 12 hours (in accordance with the working hours) duration. ICR for the Irkutsk population amounted of 3.08E-04, in Shelekhov - 4.8E-05, Sayansk - 1.1E-05. The amount of risk depends on the content offormaldehyde in all territories and chromium VI in cities of Irkutsk and Shelekhov. ICR for workers of basic occupations of studied plants in dozens of times are higher than for the urban population. Priority carcinogens are: chromium VI, nickel, formaldehyde, silicon dioxide -for the aircraft plant employees; 1,2-dichloretan, vinyl chloride - for the workers of vinyl chloride production plant; benzopyrene - for the aluminum smelter workers.
PubMed ID
29446294 View in PubMed
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Association of blood pressure and hypertension with the risk of Parkinson disease: the National FINRISK Study.

https://arctichealth.org/en/permalink/ahliterature134840
Source
Hypertension. 2011 Jun;57(6):1094-100
Publication Type
Article
Date
Jun-2011
Author
Chengxuan Qiu
Gang Hu
Miia Kivipelto
Tiina Laatikainen
Riitta Antikainen
Laura Fratiglioni
Pekka Jousilahti
Jaakko Tuomilehto
Author Affiliation
Aging Research Center, Karolinska Institutet, Gävlegatan 16, S-11330 Stockholm, Sweden. chengxuan.qiu@ki.se
Source
Hypertension. 2011 Jun;57(6):1094-100
Date
Jun-2011
Language
English
Publication Type
Article
Keywords
Adult
Age Factors
Aged
Antihypertensive Agents - therapeutic use
Blood Pressure - drug effects - physiology
Diastole
Female
Finland - epidemiology
Follow-Up Studies
Health Surveys - statistics & numerical data
Humans
Hypertension - complications - drug therapy - physiopathology
Incidence
Male
Middle Aged
Parkinson Disease - epidemiology - etiology - physiopathology
Proportional Hazards Models
Prospective Studies
Registries - statistics & numerical data
Risk Assessment - methods - statistics & numerical data
Risk factors
Sex Factors
Systole
Abstract
Cardiovascular risk factors, such as diabetes mellitus and central obesity, have been associated with Parkinson disease (PD), but data on blood pressure and PD are lacking. We sought to examine the association of blood pressure and hypertension with the risk of PD among men and women. This study consisted of 7 surveys (1972-2002) on representative samples of the general population in Finland (National FINRISK Study). A total number of 59 540 participants (age 25 to 74 years; 51.8% women) who were free of PD and stroke at baseline were prospectively followed until December 31, 2006, to identify incident PD cases using the National Social Insurance Register database. Cox proportional hazards models were constructed to estimate the hazard ratio of PD associated with blood pressure. During a mean follow-up period of 18.8 years (SD: 10.2 years), 423 men and 371 women were ascertained to have developed PD. In women, compared with normotensive subjects (
PubMed ID
21536985 View in PubMed
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Association of prenatal exposure to benzodiazepines and child internalizing problems: A sibling-controlled cohort study.

https://arctichealth.org/en/permalink/ahliterature286263
Source
PLoS One. 2017;12(7):e0181042
Publication Type
Article
Date
2017
Author
Ragnhild E Brandlistuen
Eivind Ystrom
Sonia Hernandez-Diaz
Svetlana Skurtveit
Randi Selmer
Marte Handal
Hedvig Nordeng
Source
PLoS One. 2017;12(7):e0181042
Date
2017
Language
English
Publication Type
Article
Keywords
Adult
Anxiety - chemically induced - psychology
Benzodiazepines - adverse effects
Child Behavior Disorders - chemically induced - psychology
Child, Preschool
Cohort Studies
Depression - chemically induced - psychology
Female
Gestational Age
Humans
Infant
Maternal Age
Norway
Pregnancy
Prenatal Exposure Delayed Effects - chemically induced - psychology
Risk Assessment - methods - statistics & numerical data
Risk factors
Siblings
Surveys and Questionnaires
Time Factors
Abstract
During pregnancy, many women experience sleep problems and anxiety that require treatment. The long-term safety for the child of maternal benzodiazepine (BZD) and z-hypnotic use during pregnancy remains controversial.
We conducted a cohort and a sibling control study using data from the Norwegian Mother and Child Cohort Study. Data on use of BZD and z-hypnotics, internalizing and externalizing outcomes, and covariates were collected from mothers at gestational weeks 17 and 30 and when children were 0.5, 1.5, and 3 years of age. The total sample consisted of 71,996 children (19,297 siblings) at 1.5 years and 55,081 children (13,779 siblings) at 3 years. Short-term use was defined as use in one pregnancy period only. Long-term use was defined as use in two or more pregnancy periods. Linear full cohort random-effect and sibling-matched fixed-effect regression models were used to compare internalizing and externalizing behavior in children prenatally exposed compared to those unexposed in the full cohort of pregnancies accounting for family clusters, as well as within sibling clusters comparing pregnancies with discordant exposures. Propensity score (PS) adjustment included variables on indication for use (sleep problems, symptoms of anxiety and depression) and other potential confounding factors.
Long-term prenatal exposure to BZD or z-hypnotics was associated with increased internalizing behavior in crude cohort analyses and at age 1.5 years after PS adjustment in sibling-matched fixed-effect models [ß 0.60, 95% confidence interval 0.17-0.95]. Analyses on specific drug groups showed that prenatal exposure to BZD-anxiolytics was associated with increased internalizing problems at both 1.5 years [ß 0.25, 0.01-0.49] and 3 years [ß 0.26, 0.002-0.52] while exposure to z-hypnotics was not associated with any adverse outcomes after adjustment.
The findings suggest a moderate association between BZD-anxiolytic exposure and child internalizing problems that is not likely due to stable familial confounding factors.
Notes
Cites: Monogr Neural Sci. 1983;9:119-296684207
Cites: Eur J Epidemiol. 2003;18(8):769-7112974552
Cites: Psychopharmacology (Berl). 1982;78(3):225-96818579
Cites: Epidemiology. 2011 Sep;22(5):74521811114
Cites: Int J Epidemiol. 2006 Oct;35(5):1146-5016926217
Cites: Arch Womens Ment Health. 2014 Jun;17(3):221-824442712
Cites: Epidemiology. 2016 Nov;27(6):852-827488059
Cites: Ann Med. 2002;34(2):109-1912108574
Cites: Arch Gen Psychiatry. 1993 Nov;50(11):863-708215812
Cites: Arch Gen Psychiatry. 2008 Jul;65(7):805-1518606953
Cites: Eur Child Adolesc Psychiatry. 2014 Oct;23(10):973-9224863148
Cites: Int J Epidemiol. 2015 Jun;44(3):731-426232419
Cites: J Anxiety Disord. 2008;22(3):532-917521868
Cites: Lancet. 1977 Jul 30;2(8031):24469847
Cites: Am J Obstet Gynecol. 2015 Apr;212(4):428-4125448509
Cites: Toxicol Ind Health. 2008 Feb-Mar;24(1-2):61-818818182
Cites: Neurotoxicology. 1989 Fall;10(3):501-162560534
Cites: BMC Med Res Methodol. 2008 Oct 30;8:7018973665
Cites: J Pediatr. 1977 Jan;90(1):123-6830876
Cites: BMC Med Res Methodol. 2014 Dec 17;14:13325519494
Cites: Neuropediatrics. 1992 Apr;23(2):60-71351263
Cites: Clin Pharmacol Ther. 1975 May;17(5):564-721126114
Cites: Addiction. 2015 Apr;110(4):636-4325407572
Cites: Int J Epidemiol. 2013 Dec;42(6):1702-1324163279
Cites: Reprod Toxicol. 1994 Nov-Dec;8(6):461-757881198
Cites: Prog Brain Res. 1988;73:207-282843947
Cites: Nord J Psychiatry. 2003;57(2):113-812745773
Cites: Eur J Clin Pharmacol. 2014 Nov;70(11):1367-7425204310
Cites: Pharm Weekbl Sci. 1990 Dec 14;12(6):252-51982564
Cites: Psychol Monogr. 1966;80(7):1-375968338
Cites: J Clin Epidemiol. 2013 Sep;66(9):964-7223800534
Cites: Am J Public Health. 2013 Oct;103 Suppl 1:S46-5523927516
Cites: Neuropediatrics. 1992 Feb;23(1):18-231348849
Cites: J Child Psychol Psychiatry. 1993 Mar;34(3):295-3058463369
Cites: Epidemiology. 2012 Sep;23(5):713-2022781362
Cites: Eur Child Adolesc Psychiatry. 1999 Dec;8(4):247-5410654117
Cites: Science. 1980 Jan 11;207(4427):205-77350658
Cites: Epidemiology. 1999 Jan;10(1):37-489888278
Cites: Child Dev. 2015 Mar-Apr;86(2):425-4025345342
Cites: Int J Epidemiol. 2015 Aug;44(4):1397-40725873178
Cites: Acta Obstet Gynecol Scand. 2000 Jun;79(6):435-910857866
Cites: BMC Public Health. 2012 Oct 29;12:91823107281
Cites: Paediatr Perinat Epidemiol. 2009 Nov;23(6):597-60819840297
PubMed ID
28746341 View in PubMed
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Asthmatic symptoms after exposure to ethylenebisdithiocarbamates and other pesticides in the Europit field studies.

https://arctichealth.org/en/permalink/ahliterature153966
Source
Hum Exp Toxicol. 2008 Sep;27(9):721-7
Publication Type
Article
Date
Sep-2008
Author
D. Boers
L. van Amelsvoort
C. Colosio
E. Corsini
S. Fustinoni
L. Campo
C. Bosetti
C. La Vecchia
T. Vergieva
M. Tarkowski
J. Liesivuori
P. Steerenberg
H. van Loveren
Author Affiliation
Department of Epidemiology, Maastricht University, The Netherlands.
Source
Hum Exp Toxicol. 2008 Sep;27(9):721-7
Date
Sep-2008
Language
English
Publication Type
Article
Keywords
Adult
Asthma - etiology - immunology - urine
Bulgaria
Ethylenebis(dithiocarbamates) - poisoning
Ethylenethiourea - analysis
Female
Finland
Fungicides, Industrial - poisoning
Humans
Italy
Male
Multivariate Analysis
Netherlands
Occupational Diseases - etiology - immunology - urine
Occupational Exposure - adverse effects - analysis
Odds Ratio
Pesticides - poisoning
Prospective Studies
Questionnaires
Respiratory Sounds - etiology - immunology
Risk Assessment - methods - statistics & numerical data
Abstract
We conducted a multicenter prospective study to assess the effects of occupational exposure to ethylenebisdithiocarbamate fungicides and/or other pesticides on self-reported asthma and asthmatic symptoms. This multicenter study was conducted among 248 workers exposed to pesticides and 231 non-exposed workers from five field studies. The five field studies were carried out in The Netherlands, Italy, Finland, and two studies in Bulgaria. Subjects constituting this cohort completed a self-administered questionnaire at baseline (before the start of exposure). Ethylenethiourea in urine was determined to assess exposure to ethylenebisdithiocarbamates. In multivariate analyses adjusted for all potential confounders (age, education, residence, smoking, gender, and field study), we found inverse associations, all not statistically significant, between occupational exposure to pesticides and asthma diagnosis (OR 0.41; 95% CI 0.15-1.11), complains of chest tightness (OR 0.60; 95% CI 0.36-1.02), wheeze (OR 0.56; 95% CI 0.32-0.98), asthma attack (OR 0.52; 95% CI 0.12-2.25), and asthma medication (OR 0.79; 95% CI 0.25-2.53). Furthermore, we reported null associations for multivariate analysis using ethylenethiourea as determinant for exposure. Although exposure to pesticides remains a potential health risk, our results do not suggest an association between exposure to ethylenebisdithiocarbamates and/or other pesticides used in our study on asthma and asthmatic symptoms.
PubMed ID
19042955 View in PubMed
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At-fault motor vehicle crash risk in elderly patients treated with antidepressants.

https://arctichealth.org/en/permalink/ahliterature129278
Source
Am J Geriatr Psychiatry. 2011 Dec;19(12):998-1006
Publication Type
Article
Date
Dec-2011
Author
Mark J Rapoport
Brandon Zagorski
Dallas Seitz
Nathan Herrmann
Frank Molnar
Donald A Redelmeier
Author Affiliation
University of Toronto, Toronto, Ontario, Canada. mark.rapoport@sunnybrook.ca
Source
Am J Geriatr Psychiatry. 2011 Dec;19(12):998-1006
Date
Dec-2011
Language
English
Publication Type
Article
Keywords
Accidents, Traffic - statistics & numerical data
Aged
Aged, 80 and over
Antidepressive Agents - administration & dosage - adverse effects
Automobile Driving - statistics & numerical data
Benzodiazepines - administration & dosage - adverse effects
Cholinergic Antagonists - administration & dosage - adverse effects
Drug Therapy, Combination - adverse effects
Female
Humans
Male
Ontario
Risk Assessment - methods - statistics & numerical data
Time Factors
Abstract
To assess whether antidepressant treatment is associated with a temporary increase in the risk of a motor vehicle crash among older adults.
Population-based case-only time-to-event analysis.
Data from transportation and healthcare databases for adults age 65 and older in Ontario, Canada, between January 1, 2000, and October 31, 2007. Consecutive adults who had a motor vehicle crash anytime following their 66th birthday.
The primary exposure variable was treatment with antidepressant medication, and the primary outcome measure was a motor vehicle crash.
A total of 159,678 individuals had a crash during the study, of whom 7,393 (5%) received an antidepressant in the month prior to the crash. The hazard ratio (HR) of crash associated with second-generation antidepressants was 1.10 (95% confidence interval [CI]: 1.07-1.13, ?? = 41.77, df = 1, p
PubMed ID
22123273 View in PubMed
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Biological monitoring and questionnaire for assessing exposure to ethylenebisdithiocarbamates in a multicenter European field study.

https://arctichealth.org/en/permalink/ahliterature153970
Source
Hum Exp Toxicol. 2008 Sep;27(9):681-91
Publication Type
Article
Date
Sep-2008
Author
S. Fustinoni
L. Campo
J. Liesivuori
S. Pennanen
T. Vergieva
Lgpm van Amelsvoort
C. Bosetti
H. Van Loveren
C. Colosio
Author Affiliation
Department of Occupational and Environmental Health, University of Milan and Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena, Milan, Italy. silvia.fustinoni@unimi.it
Source
Hum Exp Toxicol. 2008 Sep;27(9):681-91
Date
Sep-2008
Language
English
Publication Type
Article
Keywords
Adult
Agriculture
Bulgaria
Creatine - urine
Environmental Monitoring - methods - statistics & numerical data
Ethylenebis(dithiocarbamates) - poisoning
Ethylenethiourea - analysis
Female
Finland
Humans
Italy
Male
Middle Aged
Netherlands
Occupational Exposure - adverse effects - analysis
Occupations - classification
Questionnaires
Risk Assessment - methods - statistics & numerical data
Time Factors
Abstract
This study deals with pesticide exposure profile in some European countries with a specific focus on ethylenebisdithiocarbamates (EBDC). In all, 55 Bulgarian greenhouse workers, 51 Finnish potato farmers, 48 Italian vineyard workers, 42 Dutch floriculture farmers, and 52 Bulgarian zineb producers entered the study. Each group was matched with a group of not occupationally exposed subjects. Exposure data were gained through self-administered questionnaires and measuring ethylenethiourea (ETU) in two spot urine samples collected, respectively, before the beginning of seasonal exposure (T0), and after 30 days, at the end of the exposure period (T30). Controls underwent a similar protocol. Study agriculture workers were involved in mixing and loading pesticides, application of pesticide mixture with mechanical or manual equipments, re-entry activities, and cleaning equipments. Chemical workers were involved in synthesis, quality controls, and packing activities. The number of pesticides to whom these subjects were exposed varied from one (zineb production) to eight (potato farmers). The use of personal protective devices was variegate and regarded both aerial and dermal penetration routes. EBDC exposure, assessed by T30 urinary ETU, was found to follow the order: greenhouse workers, zineb producers, vineyard workers, potato farmers, floriculture farmers with median levels of 49.6, 23.0, 11.8, 7.5, and 0.9 microg/g creatinine; the last group having ETU at the same level of controls (approximately 0.5 microg/g creatinine). Among agriculture workers, pesticide application, especially using manual equipment, seems to be the major determinant in explaining internal dose. Although the analysis of self-administered questionnaires evidenced difficulties especially related to lack and/or poor quality of reported data, biological monitoring confirms to be a powerful tool in assessing pesticide exposure.
PubMed ID
19042950 View in PubMed
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Birth weight, childhood body mass index and risk of coronary heart disease in adults: combined historical cohort studies.

https://arctichealth.org/en/permalink/ahliterature138914
Source
PLoS One. 2010;5(11):e14126
Publication Type
Article
Date
2010
Author
Lise Geisler Andersen
Lars Angquist
Johan G Eriksson
Tom Forsen
Michael Gamborg
Clive Osmond
Jennifer L Baker
Thorkild I A Sørensen
Author Affiliation
Institute of Preventive Medicine, Copenhagen University Hospital, Copenhagen, Denmark. lg@ipm.regionh.dk
Source
PLoS One. 2010;5(11):e14126
Date
2010
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Birth Weight - physiology
Body mass index
Child
Cohort Studies
Coronary Disease - epidemiology - etiology - physiopathology
Denmark - epidemiology
Female
Finland - epidemiology
Humans
Infant, Newborn
Male
Middle Aged
Proportional Hazards Models
Registries - statistics & numerical data
Risk Assessment - methods - statistics & numerical data
Risk factors
Abstract
Low birth weight and high childhood body mass index (BMI) is each associated with an increased risk of coronary heart disease (CHD) in adult life. We studied individual and combined associations of birth weight and childhood BMI with the risk of CHD in adulthood.
Birth weight and BMI at age seven years were available in 216,771 Danish and Finnish individuals born 1924-1976. Linkage to national registers for hospitalization and causes of death identified 8,805 CHD events during up to 33 years of follow-up (median?=?24 years) after age 25 years. Analyses were conducted with Cox regression based on restricted cubic splines. Using median birth weight of 3.4 kg as reference, a non-linear relation between birth weight and CHD was found. It was not significantly different between cohorts, or between men and women, nor was the association altered by childhood BMI. For birth weights below 3.4 kg, the risk of CHD increased linearly and reached 1.28 (95% confidence limits: 1.13 to 1.44) at 2 kg. Above 3.4 kg the association weakened, and from about 4 kg there was virtually no association. BMI at age seven years was strongly positively associated with the risk of CHD and the relation was not altered by birth weight. The excess risk in individuals with a birth weight of 2.5 kg and a BMI of 17.7 kg/m(2) at age seven years was 44% (95% CI: 30% to 59%) compared with individuals with median values of birth weight (3.4 kg) and BMI (15.3 kg/m(2)).
Birth weight and BMI at age seven years appeared independently associated with the risk of CHD in adulthood. From a public health perspective we suggest that particular attention should be paid to children with a birth weight below the average in combination with excess relative weight in childhood.
Notes
Cites: Horm Metab Res. 2002 Feb;34(2):72-611972290
Cites: BMJ. 1998 Jul 25;317(7153):241-59677213
Cites: Am J Clin Nutr. 2002 Dec;76(6):1290-412450895
Cites: Int J Epidemiol. 2002 Dec;31(6):1235-912540728
Cites: J Clin Epidemiol. 2003 Feb;56(2):124-3012654406
Cites: Heart. 2004 Jan;90(1):20-414676233
Cites: BMJ. 1999 Feb 13;318(7181):427-319974455
Cites: Dan Med Bull. 1999 Jun;46(3):263-810421985
Cites: Dan Med Bull. 1999 Sep;46(4):354-710514943
Cites: Circulation. 2005 Sep 6;112(10):1414-816129799
Cites: N Engl J Med. 2005 Oct 27;353(17):1802-916251536
Cites: Obes Res. 2005 Dec;13(12):2187-9416421354
Cites: Am J Clin Nutr. 2006 Apr;83(4):767-7316600926
Cites: Clin Obstet Gynecol. 2006 Jun;49(2):270-8316721106
Cites: Stroke. 2007 Feb;38(2):264-7017218608
Cites: Int J Obes (Lond). 2007 May;31(5):777-8317060924
Cites: Am J Clin Nutr. 2007 May;85(5):1244-5017490959
Cites: Am J Epidemiol. 2007 Sep 15;166(6):634-4517456478
Cites: N Engl J Med. 2007 Dec 6;357(23):2329-3718057335
Cites: Circulation. 2008 Jan 22;117(3):405-1018172034
Cites: BMJ. 1999 Nov 27;319(7222):1403-710574856
Cites: Arch Dis Child. 2000 Mar;82(3):202-310685920
Cites: J Clin Pathol. 2000 Nov;53(11):822-811127263
Cites: Eur J Epidemiol. 2000;16(9):793-611297220
Cites: BMJ. 2001 Apr 21;322(7292):949-5311312225
Cites: Can Fam Physician. 2002 Jan;48:65-7111852614
Cites: Epidemiology. 2008 Mar;19(2):197-20318300695
Cites: Int J Epidemiol. 2008 Apr;37(2):280-918267964
Cites: Eur Heart J. 2008 Apr;29(8):1049-5618403494
Cites: J Intern Med. 2008 Jul;264(1):39-4918205766
Cites: J Clin Endocrinol Metab. 2008 Oct;93(10):3804-918628518
Cites: JAMA. 2008 Dec 24;300(24):2886-9719109117
Cites: Eur J Epidemiol. 2009;24(1):57-6119023668
Cites: Nutr Rev. 2009 May;67 Suppl 1:S12-619453665
Cites: Int J Epidemiol. 2009 Jun;38(3):656-6218719090
Cites: J Clin Endocrinol Metab. 2009 Jul;94(7):2464-7019417040
Cites: PLoS One. 2009;4(12):e819220016780
Cites: Ann Med. 2002;34(3):157-6112173685
Cites: Ann Med. 2004;36(5):389-9215478313
Cites: Lancet. 1989 Sep 9;2(8663):577-802570282
Cites: BMJ. 1993 Dec 11;307(6918):1519-248274920
Cites: Epidemiology. 1995 Jul;6(4):356-657548341
Cites: Eur J Epidemiol. 1997 Feb;13(2):133-89084994
Cites: Eur J Epidemiol. 1997 Jun;13(4):403-159258546
Cites: BMJ. 1997 Oct 4;315(7112):837-409353502
Cites: Trends Endocrinol Metab. 2002 Nov;13(9):364-812367816
PubMed ID
21124730 View in PubMed
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