Skip header and navigation

Refine By

   MORE

7 records – page 1 of 1.

Antidepressant use during pregnancy and asthma in the offspring.

https://arctichealth.org/en/permalink/ahliterature263757
Source
Pediatrics. 2015 Apr;135(4):e911-7
Publication Type
Article
Date
Apr-2015
Author
Xiaoqin Liu
Jørn Olsen
Lars Henning Pedersen
Esben Agerbo
Wei Yuan
Jiong Li
Source
Pediatrics. 2015 Apr;135(4):e911-7
Date
Apr-2015
Language
English
Publication Type
Article
Keywords
Antidepressive Agents - adverse effects - therapeutic use
Asthma - chemically induced - epidemiology
Child
Child, Preschool
Cohort Studies
Cross-Sectional Studies
Denmark
Depressive Disorder - drug therapy - epidemiology
Female
Humans
Infant
Infant, Newborn
Male
Pregnancy
Pregnancy Complications - drug therapy - epidemiology
Prenatal Exposure Delayed Effects
Proportional Hazards Models
Risk assessment
Serotonin Uptake Inhibitors - adverse effects - therapeutic use
Abstract
It has been suggested that maternal depression during pregnancy is associated with asthma in the offspring, but the role of medical treatment of depression is not known. Our goal was to examine whether prenatal antidepressant use increases the risk of asthma in the offspring.
A cohort study was performed among all live singletons born in Denmark between 1996 and 2007. Mothers who had a diagnosis of depressive disorder and/or who used antidepressants 1 year before or during the index pregnancy were identified. Using a Cox proportional hazards regression model, we estimated the hazard ratio (HR) for asthma in the offspring after antidepressant use during pregnancy.
Of the 733,685 children identified, 84,683 had a diagnosis of asthma. A total of 21,371 children were exposed to prenatal maternal depression (ie, a diagnosis of depressive disorder or use of antidepressants 1 year before or during pregnancy). Prenatal maternal depression was associated with childhood asthma (HR: 1.25 [95% confidence interval (CI): 1.20-1.30]). Overall, 8895 children were exposed to antidepressants in utero. Compared with children born to mothers with prenatal depression and no antidepressant use during pregnancy, the HR for asthma after any antidepressant use during pregnancy was 1.00 (95% CI: 0.93-1.08). HRs after use of selective serotonin reuptake inhibitors only, newer antidepressants only, and older antidepressants only were 0.95 (95% CI: 0.88-1.03), 1.11 (95% CI: 0.89-1.39), and 1.26 (95% CI: 1.02-1.55), respectively.
Antidepressant use during pregnancy generally did not increase the risk of asthma. Only use of older antidepressants was associated with an increased risk of asthma.
PubMed ID
25755245 View in PubMed
Less detail

Antidepressant use during pregnancy and psychiatric disorders in offspring: Danish nationwide register based cohort study.

https://arctichealth.org/en/permalink/ahliterature285816
Source
BMJ. 2017 Sep 06;358:j3668
Publication Type
Article
Date
Sep-06-2017
Author
Xiaoqin Liu
Esben Agerbo
Katja G Ingstrup
Katherine Musliner
Samantha Meltzer-Brody
Veerle Bergink
Trine Munk-Olsen
Source
BMJ. 2017 Sep 06;358:j3668
Date
Sep-06-2017
Language
English
Publication Type
Article
Keywords
Adolescent
Antidepressive Agents - therapeutic use
Child
Child, Preschool
Cohort Studies
Denmark - epidemiology
Disease Susceptibility
Female
Humans
Infant
Infant, Newborn
Mental Disorders - diagnosis - epidemiology
Pregnancy
Pregnancy Complications - drug therapy
Prenatal Exposure Delayed Effects
Registries
Risk factors
Withholding Treatment
Abstract
Objective To investigate the association between in utero exposure to antidepressants and risk of psychiatric disorders.Design Population based cohort study.Setting Danish national registers.Participants 905?383 liveborn singletons born during 1998-2012 in Denmark and followed from birth until July 2014, death, emigration, or date of first psychiatric diagnosis, whichever came first. The children were followed for a maximum of 16.5 years and contributed 8.1×10(6) person years at risk.Exposures for observational studies Children were categorised into four groups according to maternal antidepressant use within two years before and during pregnancy: unexposed, antidepressant discontinuation (use before but not during pregnancy), antidepressant continuation (use both before and during pregnancy), and new user (use only during pregnancy).Main outcome measure First psychiatric diagnosis in children, defined as first day of inpatient or outpatient treatment for psychiatric disorders. Hazard ratios of psychiatric disorders were estimated using Cox regression models.Results Overall, psychiatric disorders were diagnosed in 32?400 children. The adjusted 15 year cumulative incidence of psychiatric disorders was 8.0% (95% confidence interval 7.9% to 8.2%) in the unexposed group, 11.5% (10.3% to 12.9%) in the antidepressant discontinuation group, 13.6% (11.3% to 16.3%) in the continuation group, and 14.5% (10.5% to 19.8%) in the new user group. The antidepressant continuation group had an increased risk of psychiatric disorders (hazard ratio 1.27, 1.17 to 1.38), compared with the discontinuation group.Conclusions In utero exposure to antidepressants was associated with increased risk of psychiatric disorders. The association may be attributable to the severity of underlying maternal disorders in combination with antidepressant exposure in utero. The findings suggest that focusing solely on a single psychiatric disorder among offspring in studies of in utero antidepressant exposure may be too restrictive.
Notes
Cites: Neuropsychopharmacology. 2006 Jan;31(1):47-5716012532
Cites: PLoS One. 2013 Apr 25;8(4):e6303423638179
Cites: Cereb Cortex. 2017 Jun 1;27(6):3208-321627269962
Cites: Neuroscience. 2015 Jan 22;284:775-9725451292
Cites: Arch Gen Psychiatry. 2010 Aug;67(8):822-920679590
Cites: Biol Psychiatry. 2005 Aug 1;58(3):211-716084841
Cites: Scand J Public Health. 2011 Jul;39(7 Suppl):54-721775352
Cites: Clin Pharmacol Ther. 2009 Dec;86(6):672-719890255
Cites: J Clin Psychiatry. 2011 Jul;72 (7):979-8521457681
Cites: Obstet Gynecol. 2009 Sep;114(3):703-1319701065
Cites: JAMA. 2017 Apr 18;317(15):1544-155228418480
Cites: Dan Med Bull. 1999 Jun;46(3):263-810421985
Cites: Clin Epidemiol. 2013 Nov 15;5:449-5924255601
Cites: Scand J Public Health. 2011 Jul;39(7 Suppl):22-521775345
Cites: Can J Psychiatry. 2004 Nov;49(11):726-3515633850
Cites: JAMA Psychiatry. 2016 Nov 1;73(11):1163-117027732704
Cites: J Dev Behav Pediatr. 2010 Oct;31(8):641-820613624
Cites: Am J Public Health. 1998 Jan;88(1):15-99584027
Cites: J Autism Dev Disord. 2014 Oct;44(10):2558-6724803368
Cites: Arch Gen Psychiatry. 2011 Nov;68(11):1104-1221727247
Cites: J Am Acad Child Adolesc Psychiatry. 2016 May;55(5):359-6627126849
Cites: BMJ. 2016 Mar 24;352:i154727013603
Cites: PLoS One. 2015 Dec 14;10(12):e014447426657647
Cites: Epidemiology. 2001 Sep;12(5):497-50111505166
Cites: JAMA Psychiatry. 2014 May;71(5):573-8124806211
Cites: Dan Med Bull. 1998 Jun;45(3):320-39675544
Cites: Psychol Med. 2017 May 22;:1-1028528584
Cites: Scand J Public Health. 2011 Jul;39(7 Suppl):95-821775363
Cites: Am J Psychiatry. 2002 Nov;159(11):1889-9512411224
Cites: N Engl J Med. 2013 Dec 19;369(25):2406-1524350950
Cites: JAMA. 2017 Apr 18;317(15):1553-156228418479
Cites: BMJ. 2013 Apr 19;346:f205923604083
Cites: Science. 2004 Oct 29;306(5697):879-8115514160
Cites: Gen Hosp Psychiatry. 2013 May-Jun;35(3):265-7123374897
Cites: Int J Dev Neurosci. 2016 Nov;54:39-5227591973
Cites: Reprod Toxicol. 2017 Sep;72 :191-20028495514
Cites: BMJ Open. 2013 Sep 20;3(9):e00350724056487
Cites: Mol Psychiatry. 2015 Jun;20(6):727-3425155880
Cites: JAMA. 2013 Jan 2;309(1):48-5423280224
Cites: Comput Methods Programs Biomed. 2004 Jul;75(1):45-915158046
Cites: JAMA Pediatr. 2016 Feb;170(2):117-2426660917
Cites: Arch Pediatr Adolesc Med. 2006 Mar;160(3):279-8416520447
Cites: Epidemiology. 2012 Sep;23(5):713-2022781362
Cites: N Engl J Med. 2014 Jun 19;370(25):2397-40724941178
Cites: Scand J Public Health. 2011 Jul;39(7 Suppl):38-4121775349
Cites: Basic Clin Pharmacol Toxicol. 2008 Feb;102(2):245-5618226080
Cites: Int J Epidemiol. 2016 Feb;45(1):170-726748846
PubMed ID
28877907 View in PubMed
Less detail

Association of prenatal exposure to acetaminophen and coffee with childhood asthma.

https://arctichealth.org/en/permalink/ahliterature277323
Source
Pharmacoepidemiol Drug Saf. 2016 Feb;25(2):188-95
Publication Type
Article
Date
Feb-2016
Author
Xiaoqin Liu
Zeyan Liew
Jørn Olsen
Lars Henning Pedersen
Bodil Hammer Bech
Esben Agerbo
Wei Yuan
Jiong Li
Source
Pharmacoepidemiol Drug Saf. 2016 Feb;25(2):188-95
Date
Feb-2016
Language
English
Publication Type
Article
Keywords
Acetaminophen - adverse effects
Adult
Asthma - chemically induced - epidemiology - prevention & control
Coffee
Cohort Studies
Denmark - epidemiology
Female
Follow-Up Studies
Humans
Pregnancy
Prenatal Exposure Delayed Effects - chemically induced - epidemiology - prevention & control
Risk factors
Young Adult
Abstract
Some studies have suggested that maternal acetaminophen use during pregnancy is associated with asthma in the offspring, and coffee consumption may modify the toxicity of acetaminophen. We aim to examine whether pregnancy maternal acetaminophen use increases the risk for offspring asthma, and whether such a potential association could be modified by maternal coffee consumption.
We included 63,652 live-born singletons enrolled in the Danish National Birth Cohort. Maternal acetaminophen use and coffee consumption during pregnancy were assessed prospectively via the enrolment questionnaire and three computer-assisted telephone interviews. Asthma cases were identified by using the Danish National Patient Register and the Danish National Prescription Registry. We estimated the hazard ratios (HRs) for asthma according to prenatal acetaminophen and coffee exposure using Cox proportional hazards regression model.
After adjusting for potential confounders, acetaminophen use during pregnancy was associated with an increased risk of offspring asthma (HR?=?1.16, 95% confidence interval (CI): 1.11-1.22). Coffee drinking during pregnancy was associated with a slightly decreased risk (HR?=?0.94, 95%CI: 0.90-0.99). But there was no strong evidence of effect measure modification of acetaminophen use on offspring asthma by coffee consumption.
Acetaminophen use during pregnancy was associated with a modest increased risk for offspring asthma, which was not modified by coffee consumption.
PubMed ID
26676925 View in PubMed
Less detail

Depression and anxiety in the postpartum period and risk of bipolar disorder: A Danish nationwide register-based cohort study.

https://arctichealth.org/en/permalink/ahliterature283428
Source
J Clin Psychiatry. 2017 May;78(5):e469-e476
Publication Type
Article
Date
May-2017
Author
Xiaoqin Liu
Esben Agerbo
Jiong Li
Samantha Meltzer-Brody
Veerle Bergink
Trine Munk-Olsen
Source
J Clin Psychiatry. 2017 May;78(5):e469-e476
Date
May-2017
Language
English
Publication Type
Article
Keywords
Adult
Anxiety Disorders - diagnosis - epidemiology - genetics - psychology
Bipolar Disorder - diagnosis - epidemiology - genetics - psychology
Cohort Studies
Denmark
Depression, Postpartum - diagnosis - epidemiology - genetics - psychology
Female
Genetic Predisposition to Disease - genetics
Humans
Proportional Hazards Models
Puerperal Disorders - diagnosis - epidemiology - genetics - psychology
Registries
Risk factors
Abstract
The first-onset affective episode requiring inpatient treatment in the postpartum period can be a marker of bipolar disorder, but it is unknown whether milder postpartum affective episodes are also indicators of underlying bipolarity. Therefore, we aimed to study whether women with a nonpsychotic postpartum affective episode treated with antidepressants have an increased risk of bipolar disorder.
A register-based cohort study was conducted in Denmark of 122,622 parous women without psychiatric history who received a first-time antidepressant prescription during 1997-2012. We compared women with a first-time antidepressant prescription, which was our indicator of a first-onset affective disorder, within 1 year postpartum to women with a first-time antidepressant prescription outside the postpartum period. Our outcome was psychiatric contact for bipolar disorder (ICD-10 criteria) during follow-up, and we estimated hazard ratios using Cox regressions.
The risk of bipolar disorder among women with a postpartum affective episode was higher than that in women with an affective episode outside the postpartum period. The risk of bipolar disorder was 1.66 (95% CI, 1.12-2.48) for postpartum antidepressant monotherapy and 10.15 (95% CI, 7.13-14.46) for postpartum antidepressant therapy plus a subsequent prescription for anxiolytics when these therapies were compared to antidepressant monotherapy outside the postpartum period.
First-onset nonpsychotic postpartum affective disorder can be a marker of underlying bipolarity. Women who fill an antidepressant prescription following childbirth should be asked about hypomanic or manic symptoms and monitored long term. Clinically, when antidepressant monotherapy is ineffective or the individual woman experiences persistent and concerning symptoms, health professionals should consider a possible bipolar spectrum disorder.
PubMed ID
28570797 View in PubMed
Less detail

Maternal preeclampsia and childhood asthma in the offspring.

https://arctichealth.org/en/permalink/ahliterature268767
Source
Pediatr Allergy Immunol. 2015 Mar;26(2):181-5
Publication Type
Article
Date
Mar-2015
Author
Xiaoqin Liu
Jørn Olsen
Esben Agerbo
Wei Yuan
Chun Sen Wu
Jiong Li
Source
Pediatr Allergy Immunol. 2015 Mar;26(2):181-5
Date
Mar-2015
Language
English
Publication Type
Article
Keywords
Asthma - epidemiology
Case-Control Studies
Child, Preschool
Denmark - epidemiology
Female
Humans
Male
Odds Ratio
Pre-Eclampsia
Pregnancy
Prenatal Exposure Delayed Effects - epidemiology
Risk factors
Siblings
Abstract
Preeclampsia is a possible risk factor for childhood asthma in the offspring. Our aim was to find whether preeclampsia is associated with childhood asthma. We also aimed to study whether a possible association can be explained by factors shared by siblings.
All eligible live singletons born in Denmark during 1993-2007 were identified (N = 923,533), and the occurrence of preeclampsia during the index pregnancy was determined. The children were followed from their 3rd birthday to the first hospitalization, outpatient contact or prescription for asthma, emigration, death, their 18th birthday, or the end of 2010, whichever came first. We carried out a nested case-control and a case-sibling study with density sampling to estimate incidence rate ratio (IRR) of asthma as a function of maternal preeclampsia, using conditional logistic regression.
A total of 115,522 asthma cases were identified during 1996-2010. In the case-control analysis, the overall IRR of asthma for those exposed to maternal preeclampsia was 1.19 (95% confidence interval (CI): 1.15, 1.24). The IRRs for asthma according to early and late onset preeclampsia were 1.88 (95% CI: 1.67, 2.11) and 1.14 (95% CI: 1.10, 1.19). In the case-sibling analysis, the corresponding IRRs were 1.06 (95% CI: 0.98, 1.14), 1.15 (95% CI: 1.02, 1.29), and 1.02 (95% CI: 0.93, 1.11), respectively.
Early onset preeclampsia was associated with an increased risk of asthma in the offspring, but part of this association may be due to confounding by factors shared by siblings.
PubMed ID
25643931 View in PubMed
Less detail

Prenatal stress and childhood asthma in the offspring: role of age at onset.

https://arctichealth.org/en/permalink/ahliterature276393
Source
Eur J Public Health. 2015 Dec;25(6):1042-6
Publication Type
Article
Date
Dec-2015
Author
Xiaoqin Liu
Jørn Olsen
Esben Agerbo
Wei Yuan
Torben Sigsgaard
Jiong Li
Source
Eur J Public Health. 2015 Dec;25(6):1042-6
Date
Dec-2015
Language
English
Publication Type
Article
Keywords
Adolescent
Age of Onset
Asthma - epidemiology
Bereavement
Child
Child, Preschool
Cohort Studies
Denmark - epidemiology
Female
Humans
Infant
Infant, Newborn
Male
Mothers - psychology
Pregnancy
Pregnancy Complications - epidemiology
Proportional Hazards Models
Risk factors
Stress, Psychological - epidemiology
Abstract
Asthma is a heterogeneous disorder with different phenotypes, and age at onset may define part of them. Little is known about possible association between prenatal stress and asthma phenotypes according to age at onset. We aim to investigate whether there is an association between prenatal stress and asthma, and if so, whether such an association differs according to age at asthma onset.
We carried out a cohort study based on several national registers in Denmark, including all live singletons born during 1996-2007 in Denmark (N = 750,058). We identified children born to mothers who lost a close relative (a child, partner/spouse, a parent or a sibling) 1 year prior to or during pregnancy as the bereaved group. Using Cox proportional hazards regression model, we evaluated the hazard ratios (HRs) for asthma in children of bereaved mothers, compared with children of non-bereaved mothers.
Prenatal stress following maternal bereavement was associated with a marginally increased risk of asthma events in children aged 0-3 years [HR = 1.04, 95% confidence interval (CI): 1.00-1.07], while unexpected bereavement was associated with a higher risk (HR = 1.13, 95% CI: 1.02-1.24). There was no association between prenatal bereavement and asthma in children aged 4-15 years (HR = 1.02, 95% CI: 0.96-1.09).
Prenatal stress is possibly associated with asthma events in children aged 0-3 years, but not with asthma in children aged 4-15 years irrespective of age at asthma onset.
PubMed ID
26116689 View in PubMed
Less detail

Psychological stress and hospitalization for childhood asthma-a nationwide cohort study in two Nordic countries.

https://arctichealth.org/en/permalink/ahliterature106268
Source
PLoS One. 2013;8(10):e78816
Publication Type
Article
Date
2013
Author
Xiaoqin Liu
Jørn Olsen
Esben Agerbo
Wei Yuan
Sven Cnattingius
Mika Gissler
Jiong Li
Author Affiliation
Section for Epidemiology, Department of Public Health, Aarhus University, Aarhus, Denmark ; Department of Epidemiology and Social Science on Reproductive Health, Shanghai Institute of Planned Parenthood Research, WHO Collaborating Center for Research in Human Reproduction, National Population & Family Planning Key Laboratory of Contraceptive Drugs and Devices, Shanghai, China.
Source
PLoS One. 2013;8(10):e78816
Date
2013
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Asthma - epidemiology - psychology - therapy
Bereavement
Child
Child, Preschool
Cohort Studies
Denmark - epidemiology
Female
Hospitalization - statistics & numerical data
Humans
Infant
Infant, Newborn
Male
Middle Aged
Pregnancy
Stress, Psychological - epidemiology
Sweden - epidemiology
Young Adult
Abstract
Exposures to psychological stress in early life may contribute to the development or exacerbation of asthma. We undertook a cohort study based on data from several population-based registers in Denmark and Sweden to examine whether bereavement in childhood led to increased asthma hospitalization.
All singleton children born in Denmark during 1977-2008 and in Sweden during 1973-2006 were included in the study (N=5,202,576). The children were followed from birth to the date of first asthma hospitalization, emigration, death, their 18(th) birthday, or the end of study (31 December 2007 in Sweden and 31 December 2008 in Denmark), whichever came first. All the children were assigned to the non-bereaved group until they lost a close relative (mother, father or a sibling), from when they were included in the bereaved group. We evaluated the hazard ratio (HR) of first hospitalization for asthma in bereaved children using Cox proportional hazards regression models, compared to those who were in the non-bereaved group. We also did a sub-analysis on the association between bereavement and first asthma medication.
A total of 147,829 children were hospitalized for asthma. The overall adjusted HR of asthma hospitalization in bereaved children was 1.10 (95% confidence interval (CI): 1.04-1.16), compared to non-bereaved children. The risk of asthma hospitalization was increased in those who lost a close relative at age of 14-17 years (HR=1.54, 95% CI: 1.23-1.92), but not in younger age groups. The association between bereavement and asthma hospitalization did not change over time since bereavement. In the sub-analysis in singleton live births during 1996-2008 recorded in the DMBR, bereavement was associated with a lower use of asthma medication (HR=0.87, 95% CI: 0.80-0.95).
Our data suggests that psychological stress following bereavement in late adolescence is associated with an increased risk of asthma hospitalization or lowers the threshold for asthma hospitalization.
Notes
Cites: Science. 2000 Mar 31;287(5462):2398-910766613
Cites: PLoS One. 2012;7(5):e3632822606255
Cites: Arch Pediatr Adolesc Med. 2001 Mar;155(3):401-611231809
Cites: Am J Respir Crit Care Med. 2002 Feb 1;165(3):358-6511818321
Cites: Ambul Pediatr. 2001 Jul-Aug;1(4):185-9311888399
Cites: J Allergy Clin Immunol. 2002 Jun;109(6):923-812063519
Cites: JAMA. 2002 Sep 11;288(10):1269-7812215135
Cites: Biol Psychiatry. 2002 Oct 15;52(8):776-8412372649
Cites: Am J Prev Med. 2003 Feb;24(2):160-912568822
Cites: BMJ. 1998 Mar 21;316(7135):931-39552851
Cites: Dan Med Bull. 1999 Jun;46(3):263-810421985
Cites: Dan Med Bull. 1999 Sep;46(4):354-710514943
Cites: Immunol Allergy Clin North Am. 2005 Feb;25(1):83-10515579366
Cites: Curr Opin Allergy Clin Immunol. 2005 Feb;5(1):23-915643340
Cites: J Sch Health. 2006 Jan;76(1):18-2416457681
Cites: Arch Pediatr Adolesc Med. 2006 Mar;160(3):279-8416520447
Cites: J Pediatr. 2006 May;148(5):637-64116737876
Cites: J Allergy Clin Immunol. 2006 Sep;118(3):543-8; quiz 549-5016950268
Cites: N Engl J Med. 2006 Nov 23;355(21):2226-3517124020
Cites: Dan Med Bull. 2006 Nov;53(4):441-917150149
Cites: Respir Med. 2007 Jan;101(1):107-1716735111
Cites: Int J Epidemiol. 2007 Jun;36(3):569-7917329314
Cites: Am J Respir Crit Care Med. 2008 Jan 15;177(2):142-717932381
Cites: Psychosom Med. 2012 Jul-Aug;74(6):635-4122753636
Cites: PLoS One. 2012;7(8):e4092122870208
Cites: Am J Respir Crit Care Med. 2013 Jan 15;187(2):144-5222955315
Cites: Lancet. 2000 Sep 16;356(9234):982-711041399
Cites: J Allergy Clin Immunol. 2004 Jan;113(1):101-814713914
Cites: Pediatrics. 2004 Feb;113(2):229-3714754931
Cites: Chest. 2004 May;125(5):1680-415136376
Cites: J Allergy Clin Immunol. 2004 Jun;113(6):1051-715208584
Cites: J Pediatr Psychol. 2004 Oct;29(7):475-9115347697
Cites: N Engl J Med. 1995 Jan 19;332(3):133-87800004
Cites: BMC Health Serv Res. 2008;8:1618211673
Cites: Arch Pediatr Adolesc Med. 2009 Mar;163(3):244-5019255392
Cites: Am J Hum Biol. 2009 Jul-Aug;21(4):488-50019309684
Cites: Eur J Epidemiol. 2009;24(11):659-6719504049
Cites: J Asthma. 2010 Feb;47(1):100-420100028
Cites: Respir Res. 2010;11:1120113468
Cites: J Epidemiol Community Health. 2010 Jul;64(7):636-4219828512
Cites: J Urban Health. 2010 Jul;87(4):688-70220499191
Cites: Eur Respir J. 2010 Dec;36(6):1400-920413538
Cites: J Allergy Clin Immunol. 2011 Mar;127(3):734-40.e1-721194742
Cites: Eur Respir J. 2011 Jun;37(6):1360-521030455
Cites: Scand J Public Health. 2011 Jul;39(7 Suppl):38-4121775349
Cites: J Allergy Clin Immunol. 2011 Aug;128(2):337-45.e121704362
Cites: Omega (Westport). 2011;63(3):271-9021928600
Cites: Int J Epidemiol. 2011 Oct;40(5):1161-720675718
Cites: PLoS One. 2011;6(11):e2720222087265
Cites: Eur Respir Rev. 2013 Mar 1;22(127):44-5223457164
PubMed ID
24205324 View in PubMed
Less detail

7 records – page 1 of 1.