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Mortality Among Hardmetal Production Workers: Occupational Exposures.

https://arctichealth.org/en/permalink/ahliterature294339
Source
J Occup Environ Med. 2017 Dec; 59(12):e297-e305
Publication Type
Journal Article
Multicenter Study
Date
Dec-2017
Author
Kathleen J Kennedy
Nurtan A Esmen
Jeanine M Buchanich
Sarah Zimmerman
Anne J Sleeuwenhoek
Gary M Marsh
Author Affiliation
Division of Environmental and Occupational Health Sciences, School of Public Health, University of Illinois at Chicago, Chicago, Illinois (Drs Kennedy, Esmen); Center for Occupational Biostatistics and Epidemiology, Department of Biostatistics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pennsylvania (Dr Buchanich, Ms Zimmerman, Dr Marsh); Institute of Occupational Medicine, Edinburgh, UK (Dr Sleeuwenhoek).
Source
J Occup Environ Med. 2017 Dec; 59(12):e297-e305
Date
Dec-2017
Language
English
Publication Type
Journal Article
Multicenter Study
Keywords
Air Pollutants, Occupational - analysis
Alloys - adverse effects - analysis
Austria
Chemical Industry - statistics & numerical data
Cobalt - adverse effects - analysis
Cohort Studies
Germany
Humans
Occupational Exposure - analysis
Retrospective Studies
Sweden
Tungsten - adverse effects - analysis
United Kingdom
United States
Abstract
To generate quantitative exposure estimates for use in retrospective occupational cohort mortality studies of the hardmetal industry.
Job-exposure matrices (JEMs) were constructed for cobalt, tungsten, and nickel over the time period 1952 to 2014. The JEMs consisted of job class categories, based on job titles and processes performed, and exposure estimates calculated from available company industrial hygiene measurements.
Exposure intervals of one-half order magnitude were established for all three agents. Eight job classes had significantly decreasing time trends for cobalt exposure; no significant time trends were detected for tungsten or nickel exposures.
The levels of exposures determined for this study were similar to or lower than those previously reported for the hardmetal industry during the 1952 to 2014 study period.
PubMed ID
28704227 View in PubMed
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Paternal and maternal obesity but not gestational weight gain is associated with type 1 diabetes.

https://arctichealth.org/en/permalink/ahliterature298630
Source
Int J Epidemiol. 2018 04 01; 47(2):417-426
Publication Type
Journal Article
Multicenter Study
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Date
04-01-2018
Author
Maria C Magnus
Sjurdur F Olsen
Charlotta Granstrom
Nicolai A Lund-Blix
Jannet Svensson
Jesper Johannesen
Abigail Fraser
Torild Skrivarhaug
Geir Joner
Pål R Njølstad
Ketil Størdal
Lars C Stene
Author Affiliation
Division for Mental and Physical Health, Norwegian Institute of Public Health, Oslo, Norway.
Source
Int J Epidemiol. 2018 04 01; 47(2):417-426
Date
04-01-2018
Language
English
Publication Type
Journal Article
Multicenter Study
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Keywords
Adolescent
Adult
Body mass index
Child
Cohort Studies
Denmark - epidemiology
Diabetes Mellitus, Type 1 - epidemiology
Female
Gestational Weight Gain
Humans
Incidence
Male
Norway - epidemiology
Obesity - epidemiology
Parents
Pregnancy
Prenatal Exposure Delayed Effects
Proportional Hazards Models
Risk factors
Young Adult
Abstract
Our objective was to examine the associations of parental body mass index (BMI) and maternal gestational weight gain with childhood-onset type 1 diabetes. Comparing the associations of maternal and paternal BMI with type 1 diabetes in the offspring will provide further insight into the role of unmeasured confounding by characteristics linked to BMI in both parents.
We studied 132 331 children participating in the Norwegian Mother and Child Cohort Study (MoBa) and the Danish National Birth Cohort (DNBC) who were born between February 1998 and July 2009. Exposures of interest included parental BMI and maternal gestational weight gain obtained by maternal report. We used Cox-proportional hazards regression to examine the risk of type 1 diabetes (n=499 cases), which was ascertained by national childhood diabetes registers.
The incidence of type 1 diabetes was 32.7 per 100 000 person-years in MoBa and 28.5 per 100 000 person-years in DNBC. Both maternal pre-pregnancy obesity, adjusted hazard ratio (HR) 1.41 [95% confidence interval (CI): 1.06, 1.89] and paternal obesity, adjusted HR 1.51 (95% CI: 1.11, 2.04), were associated with childhood-onset type 1 diabetes. The associations were similar after mutual adjustment. In contrast, maternal total gestational weight gain was not associated with childhood-onset type 1 diabetes, adjusted HR 1.00 (95% CI: 0.99, 1.02) per kilogram increase.
Our study suggests that the association between maternal obesity and childhood-onset type 1 diabetes is not likely explained by intrauterine mechanisms, but possibly rather by unknown environmental factors influencing BMI in the family.
PubMed ID
29415279 View in PubMed
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Thermal perception thresholds among workers in a cold climate.

https://arctichealth.org/en/permalink/ahliterature295084
Source
Int Arch Occup Environ Health. 2017 10; 90(7):645-652
Publication Type
Journal Article
Multicenter Study
Research Support, Non-U.S. Gov't
Date
10-2017
Author
Lage Burström
Bodil Björ
Tohr Nilsson
Hans Pettersson
Ingemar Rödin
Jens Wahlström
Author Affiliation
Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine, Umeå University, 901 87, Umeå, Sweden. lage.burstrom@gmail.com.
Source
Int Arch Occup Environ Health. 2017 10; 90(7):645-652
Date
10-2017
Language
English
Publication Type
Journal Article
Multicenter Study
Research Support, Non-U.S. Gov't
Keywords
Adolescent
Adult
Age Factors
Arctic Regions
Cold Climate - adverse effects
Cross-Sectional Studies
Diabetes Mellitus - epidemiology
Female
Fingers - physiopathology
Hand - physiopathology
Humans
Male
Middle Aged
Norway
Residence Characteristics
Sensory Thresholds - physiology
Sex Factors
Smoking - epidemiology
Sweden
Vibration - adverse effects
Young Adult
Abstract
To investigate whether exposure to cold could influence the thermal perception thresholds in a working population.
This cross-sectional study was comprised of 251 males and females and was carried out at two mines in the northern part of Norway and Sweden. The testing included a baseline questionnaire, a clinical examination and measurements of thermal perception thresholds, on both hands, the index (Digit 2) and little (Digit 5) fingers, for heat and cold.
The thermal perception thresholds were affected by age, gender and test site. The thresholds were impaired by experiences of frostbite in the fingers and the use of medication that potentially could affect neurosensory functions. No differences were found between the calculated normative values for these workers and those in other comparative investigations conducted in warmer climates.
The study provided no support for the hypothesis that living and working in cold climate will lead to impaired thermal perception thresholds. Exposure to cold that had caused localized damage in the form of frostbite was shown to lead to impaired thermal perception.
Notes
Cites: Int Arch Occup Environ Health. 2011 Mar;84(3):325-34 PMID 20496077
Cites: JAMA. 2015 Nov 24;314(20):2172-81 PMID 26599185
Cites: Clin Neurophysiol. 2010 Nov;121(11):1878-85 PMID 20478739
Cites: Int J Circumpolar Health. 2014 Feb 17;73:null PMID 24624368
Cites: Clin J Pain. 2006 Sep;22(7):610-6 PMID 16926576
Cites: Muscle Nerve. 2007 Feb;35(2):189-95 PMID 17094098
Cites: Pain. 2006 Aug;123(3):231-43 PMID 16697110
Cites: Eur J Appl Physiol. 2004 Jun;92(1-2):62-8 PMID 14991327
Cites: Int Arch Occup Environ Health. 2008 Apr;81(5):535-43 PMID 17901976
Cites: Muscle Nerve. 1998 Mar;21(3):367-74 PMID 9486866
Cites: Eur J Appl Physiol. 2002 Mar;86(5):418-27 PMID 11882928
Cites: Neurotoxicol Teratol. 1994 Jan-Feb;16(1):105-12 PMID 8183183
Cites: J Neurol Neurosurg Psychiatry. 1976 Nov;39(11):1071-5 PMID 188989
Cites: Int Arch Occup Environ Health. 2008 Apr;81(5):519-33 PMID 18180945
Cites: Ind Health. 2002 Oct;40(4):353-61 PMID 12502238
Cites: J Clin Neurophysiol. 1999 Sep;16(5):462-71 PMID 10576229
Cites: Occup Environ Med. 2001 Jul;58(7):472-8 PMID 11404453
Cites: Muscle Nerve. 2016 May;53(5):671-82 PMID 26872938
Cites: J Peripher Nerv Syst. 2005 Dec;10(4):354-8 PMID 16279984
Cites: Clin Neurophysiol. 2013 Aug;124(8):1680-8 PMID 23507585
Cites: Brain Behav. 2016 May 17;6(7):e00466 PMID 27458540
Cites: Eur J Pain. 2006 Jan;10(1):77-88 PMID 16291301
Cites: J Clin Neurosci. 2015 Mar;22(3):588-91 PMID 25624058
Cites: J Peripher Nerv Syst. 2013 Mar;18(1):7-18 PMID 23521638
Cites: Int Arch Occup Environ Health. 2002 Jan;75(1-2):90-6 PMID 11898882
Cites: J Neurol Neurosurg Psychiatry. 1989 Sep;52(9):1072-7 PMID 2795077
Cites: Ind Health. 2000 Oct;38(4):366-71 PMID 11061479
Cites: Pain. 2015 Nov;156(11):2203-11 PMID 26075963
Cites: Int Arch Occup Environ Health. 2002 Jan;75(1-2):43-54 PMID 11898876
Cites: Zhonghua Yi Xue Za Zhi (Taipei). 1999 Jul;62(7):431-7 PMID 10418177
Cites: Int Arch Occup Environ Health. 2017 Apr 11;:null PMID 28401298
Cites: Diabetologia. 1985 Mar;28(3):131-7 PMID 3996794
Cites: Scand J Work Environ Health. 2016 Jan;42(1):61-70 PMID 26473467
Cites: Scand J Work Environ Health. 1990 Oct;16(5):334-9 PMID 2255874
Cites: Pain. 1998 Feb;74(2-3):275-86 PMID 9520242
PubMed ID
28497276 View in PubMed
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Persistent Environmental Toxicants in Breast Milk and Rapid Infant Growth.

https://arctichealth.org/en/permalink/ahliterature289484
Source
Ann Nutr Metab. 2017; 70(3):210-216
Publication Type
Journal Article
Multicenter Study
Research Support, Non-U.S. Gov't
Date
2017
Author
Rachel Criswell
Virissa Lenters
Siddhartha Mandal
Hein Stigum
Nina Iszatt
Merete Eggesbø
Author Affiliation
Department of Environmental Exposure and Epidemiology, Norwegian Institute of Public Health, Oslo, Norway.
Source
Ann Nutr Metab. 2017; 70(3):210-216
Date
2017
Language
English
Publication Type
Journal Article
Multicenter Study
Research Support, Non-U.S. Gov't
Keywords
Adult
Bayes Theorem
Birth weight
Body mass index
Body Weight - physiology
Cohort Studies
Female
Gestational Age
Growth - physiology
Humans
Infant
Infant, Newborn
Logistic Models
Male
Maternal Age
Maternal Exposure - adverse effects
Metals, Heavy - analysis - toxicity
Milk, human - chemistry
Norway
Obesity - physiopathology
Pesticides - analysis - toxicity
Polychlorinated Biphenyls - analysis - toxicity
Pregnancy
Pregnancy Complications - physiopathology
Prenatal Exposure Delayed Effects - chemically induced - physiopathology
Abstract
Many environmental toxicants are passed to infants in utero and through breast milk. Exposure to toxicants during the perinatal period can alter growth patterns, impairing growth or increasing obesity risk. Previous studies have focused on only a few toxicants at a time, which may confound results. We investigated levels of 26 toxicants in breast milk and their associations with rapid infant growth, a risk factor for later obesity.
We used data from the Norwegian HUMIS study, a multi-center cohort of 2,606 mothers and newborns enrolled between 2002 and 2008. Milk samples collected 1 month after delivery from a subset of 789 women oversampled by overweight were analyzed for toxicants including polychlorinated biphenyls (PCBs), heavy metals, and pesticides. Growth was defined as change in weight-for-age z-score between 0 and 6 months among the HUMIS population, and rapid growth was defined as change in z-score above 0.67. We used a Bayesian variable selection method to determine the exposures that most explained variation in the outcome. Identified toxicants were included in logistic and linear regression models to estimate associations with growth, adjusting for maternal age, smoking, education, pre-pregnancy body mass index (BMI), gestational weight gain, parity, child sex, cumulative breastfeeding, birth weight, gestational age, and preterm status.
Of 789 infants, 19.2% displayed rapid growth. The median maternal age was 29.6 years, and the median pre-pregnancy BMI was 24.0 kg/m2, with 45.3% of mothers overweight or obese. Rapid growers were more likely to be firstborn. Hexachlorobenzene, ß-hexachlorocyclohexane (ß-HCH), and PCB-74 were identified in the variable selection method. An interquartile range (IQR) increase in ß-HCH exposure was associated with a lower odds of rapid growth (OR 0.63, 95% CI 0.42-0.94). Newborns exposed to high levels of ß-HCH showed reduced infant growth (ß = -0.03, 95% CI -0.05 to -0.01 for IQR increase in breast milk concentration). No other significant associations were found.
Our results suggest that early life ß-HCH exposure may be linked to slowed growth. Further research is warranted on the potential mechanism behind this association and the longer-term metabolic effects of perinatal ß-HCH exposure.
PubMed ID
28301833 View in PubMed
Less detail

Persistent Environmental Toxicants in Breast Milk and Rapid Infant Growth.

https://arctichealth.org/en/permalink/ahliterature289642
Source
Ann Nutr Metab. 2017; 70(3):210-216
Publication Type
Journal Article
Multicenter Study
Research Support, Non-U.S. Gov't
Date
2017
Author
Rachel Criswell
Virissa Lenters
Siddhartha Mandal
Hein Stigum
Nina Iszatt
Merete Eggesbø
Author Affiliation
Department of Environmental Exposure and Epidemiology, Norwegian Institute of Public Health, Oslo, Norway.
Source
Ann Nutr Metab. 2017; 70(3):210-216
Date
2017
Language
English
Publication Type
Journal Article
Multicenter Study
Research Support, Non-U.S. Gov't
Keywords
Adult
Bayes Theorem
Birth weight
Body mass index
Body Weight - physiology
Cohort Studies
Female
Gestational Age
Growth - physiology
Humans
Infant
Infant, Newborn
Logistic Models
Male
Maternal Age
Maternal Exposure - adverse effects
Metals, Heavy - analysis - toxicity
Milk, human - chemistry
Norway
Obesity - physiopathology
Pesticides - analysis - toxicity
Polychlorinated Biphenyls - analysis - toxicity
Pregnancy
Pregnancy Complications - physiopathology
Prenatal Exposure Delayed Effects - chemically induced - physiopathology
Abstract
Many environmental toxicants are passed to infants in utero and through breast milk. Exposure to toxicants during the perinatal period can alter growth patterns, impairing growth or increasing obesity risk. Previous studies have focused on only a few toxicants at a time, which may confound results. We investigated levels of 26 toxicants in breast milk and their associations with rapid infant growth, a risk factor for later obesity.
We used data from the Norwegian HUMIS study, a multi-center cohort of 2,606 mothers and newborns enrolled between 2002 and 2008. Milk samples collected 1 month after delivery from a subset of 789 women oversampled by overweight were analyzed for toxicants including polychlorinated biphenyls (PCBs), heavy metals, and pesticides. Growth was defined as change in weight-for-age z-score between 0 and 6 months among the HUMIS population, and rapid growth was defined as change in z-score above 0.67. We used a Bayesian variable selection method to determine the exposures that most explained variation in the outcome. Identified toxicants were included in logistic and linear regression models to estimate associations with growth, adjusting for maternal age, smoking, education, pre-pregnancy body mass index (BMI), gestational weight gain, parity, child sex, cumulative breastfeeding, birth weight, gestational age, and preterm status.
Of 789 infants, 19.2% displayed rapid growth. The median maternal age was 29.6 years, and the median pre-pregnancy BMI was 24.0 kg/m2, with 45.3% of mothers overweight or obese. Rapid growers were more likely to be firstborn. Hexachlorobenzene, ß-hexachlorocyclohexane (ß-HCH), and PCB-74 were identified in the variable selection method. An interquartile range (IQR) increase in ß-HCH exposure was associated with a lower odds of rapid growth (OR 0.63, 95% CI 0.42-0.94). Newborns exposed to high levels of ß-HCH showed reduced infant growth (ß = -0.03, 95% CI -0.05 to -0.01 for IQR increase in breast milk concentration). No other significant associations were found.
Our results suggest that early life ß-HCH exposure may be linked to slowed growth. Further research is warranted on the potential mechanism behind this association and the longer-term metabolic effects of perinatal ß-HCH exposure.
PubMed ID
28301833 View in PubMed
Less detail