Heme oxygenase 1 polymorphism, occupational vapor, gas, dust, and fume exposure and chronic obstructive pulmonary disease in a Danish population-based study

Else Toft Würtz, Charlotte Brasch-Andersen, Rudi Steffensen, Jens Georg Hansen, Tine Halsen Malling, Vivi Schlünssen, Øyvind Omland

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Resumé

Objectives The number of dinucleotide repeats (GT) nmodulate expression of heme oxygenase 1 (HMOX1), a stress response gene. Multiple repeats might affect chronic obstructive pulmonary disease (COPD) susceptibility. We aimed to investigate the association of this polymorphism with COPD and its interaction with occupational exposures (vapor, gas, dust, or fumes). Methods This population-based cross-sectional study included 4703 Danes, aged 45-84 years. HMOX1 (GT) nwas genotyped and grouped as short: ≤26, medium: 27-32 and long: ≥33 alleles. COPD was defined by the lower limit of normal (2.5 thFEV 1/FVC and FEV 1centiles). Occupational exposure was defined as ever exposed to vapor, gas, dust, or fume in expert-selected jobs. Associations were analyzed by adjusted mixed logistic regression. Results The population included 6% with COPD, 48% who had smoked ≥10 pack-years, and 46% with occupational exposure. HMOX1 was genotyped in 4423 participants. The adjusted odds ratio (OR) for the association between HMOX1 long allele and COPD was 1.75 [95% confidence interval (CI) 1.18-2.60]. An interaction was evident between HMOX1 long allele and occupational exposure, OR 2.38 (95% CI 1.04-5.46), versus HMOX1 short/medium without exposure. Analyses were replicated in another cohort, aged 20-44 years, N=1168, including 3% with COPD, 25% who had smoked ≥10 pack-years and 20% with occupational exposure. No associations were seen between COPD and HMOX1 long allele here. Conclusions Long alleles in HMOX1 alone and in interaction with occupational exposure seem to be associated with COPD. Failure to replicate data may be due to premature age for COPD development and low occupational exposure prevalence. We propose this long allele may be a genetic contributor to the COPD pathogenesis.

OriginalsprogEngelsk
TidsskriftScandinavian Journal of Work, Environment & Health
ISSN0355-3140
DOI
StatusE-pub ahead of print - 11 aug. 2019

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Pulmonary diseases
Heme Oxygenase-1
Fumes
Polymorphism
Dust
Chronic Obstructive Pulmonary Disease
polymorphism
occupational exposure
Gases
Vapors
Occupational Exposure
dust
Disease
allele
gas
Population
Alleles
confidence interval
interaction
confidence

Citer dette

@article{bef0a7333f374f56ac2bdcf600eb94db,
title = "Heme oxygenase 1 polymorphism, occupational vapor, gas, dust, and fume exposure and chronic obstructive pulmonary disease in a Danish population-based study",
abstract = "Objectives The number of dinucleotide repeats (GT) nmodulate expression of heme oxygenase 1 (HMOX1), a stress response gene. Multiple repeats might affect chronic obstructive pulmonary disease (COPD) susceptibility. We aimed to investigate the association of this polymorphism with COPD and its interaction with occupational exposures (vapor, gas, dust, or fumes). Methods This population-based cross-sectional study included 4703 Danes, aged 45-84 years. HMOX1 (GT) nwas genotyped and grouped as short: ≤26, medium: 27-32 and long: ≥33 alleles. COPD was defined by the lower limit of normal (2.5 thFEV 1/FVC and FEV 1centiles). Occupational exposure was defined as ever exposed to vapor, gas, dust, or fume in expert-selected jobs. Associations were analyzed by adjusted mixed logistic regression. Results The population included 6{\%} with COPD, 48{\%} who had smoked ≥10 pack-years, and 46{\%} with occupational exposure. HMOX1 was genotyped in 4423 participants. The adjusted odds ratio (OR) for the association between HMOX1 long allele and COPD was 1.75 [95{\%} confidence interval (CI) 1.18-2.60]. An interaction was evident between HMOX1 long allele and occupational exposure, OR 2.38 (95{\%} CI 1.04-5.46), versus HMOX1 short/medium without exposure. Analyses were replicated in another cohort, aged 20-44 years, N=1168, including 3{\%} with COPD, 25{\%} who had smoked ≥10 pack-years and 20{\%} with occupational exposure. No associations were seen between COPD and HMOX1 long allele here. Conclusions Long alleles in HMOX1 alone and in interaction with occupational exposure seem to be associated with COPD. Failure to replicate data may be due to premature age for COPD development and low occupational exposure prevalence. We propose this long allele may be a genetic contributor to the COPD pathogenesis.",
author = "W{\"u}rtz, {Else Toft} and Charlotte Brasch-Andersen and Rudi Steffensen and Hansen, {Jens Georg} and Malling, {Tine Halsen} and Vivi Schl{\"u}nssen and {\O}yvind Omland",
year = "2019",
month = "8",
day = "11",
doi = "10.5271/sjweh.3846",
language = "English",
journal = "Scandinavian Journal of Work, Environment & Health",
issn = "0355-3140",
publisher = "Tyoterveyslaitos",

}

Heme oxygenase 1 polymorphism, occupational vapor, gas, dust, and fume exposure and chronic obstructive pulmonary disease in a Danish population-based study. / Würtz, Else Toft; Brasch-Andersen, Charlotte; Steffensen, Rudi; Hansen, Jens Georg; Malling, Tine Halsen; Schlünssen, Vivi; Omland, Øyvind.

I: Scandinavian Journal of Work, Environment & Health, 11.08.2019.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

TY - JOUR

T1 - Heme oxygenase 1 polymorphism, occupational vapor, gas, dust, and fume exposure and chronic obstructive pulmonary disease in a Danish population-based study

AU - Würtz, Else Toft

AU - Brasch-Andersen, Charlotte

AU - Steffensen, Rudi

AU - Hansen, Jens Georg

AU - Malling, Tine Halsen

AU - Schlünssen, Vivi

AU - Omland, Øyvind

PY - 2019/8/11

Y1 - 2019/8/11

N2 - Objectives The number of dinucleotide repeats (GT) nmodulate expression of heme oxygenase 1 (HMOX1), a stress response gene. Multiple repeats might affect chronic obstructive pulmonary disease (COPD) susceptibility. We aimed to investigate the association of this polymorphism with COPD and its interaction with occupational exposures (vapor, gas, dust, or fumes). Methods This population-based cross-sectional study included 4703 Danes, aged 45-84 years. HMOX1 (GT) nwas genotyped and grouped as short: ≤26, medium: 27-32 and long: ≥33 alleles. COPD was defined by the lower limit of normal (2.5 thFEV 1/FVC and FEV 1centiles). Occupational exposure was defined as ever exposed to vapor, gas, dust, or fume in expert-selected jobs. Associations were analyzed by adjusted mixed logistic regression. Results The population included 6% with COPD, 48% who had smoked ≥10 pack-years, and 46% with occupational exposure. HMOX1 was genotyped in 4423 participants. The adjusted odds ratio (OR) for the association between HMOX1 long allele and COPD was 1.75 [95% confidence interval (CI) 1.18-2.60]. An interaction was evident between HMOX1 long allele and occupational exposure, OR 2.38 (95% CI 1.04-5.46), versus HMOX1 short/medium without exposure. Analyses were replicated in another cohort, aged 20-44 years, N=1168, including 3% with COPD, 25% who had smoked ≥10 pack-years and 20% with occupational exposure. No associations were seen between COPD and HMOX1 long allele here. Conclusions Long alleles in HMOX1 alone and in interaction with occupational exposure seem to be associated with COPD. Failure to replicate data may be due to premature age for COPD development and low occupational exposure prevalence. We propose this long allele may be a genetic contributor to the COPD pathogenesis.

AB - Objectives The number of dinucleotide repeats (GT) nmodulate expression of heme oxygenase 1 (HMOX1), a stress response gene. Multiple repeats might affect chronic obstructive pulmonary disease (COPD) susceptibility. We aimed to investigate the association of this polymorphism with COPD and its interaction with occupational exposures (vapor, gas, dust, or fumes). Methods This population-based cross-sectional study included 4703 Danes, aged 45-84 years. HMOX1 (GT) nwas genotyped and grouped as short: ≤26, medium: 27-32 and long: ≥33 alleles. COPD was defined by the lower limit of normal (2.5 thFEV 1/FVC and FEV 1centiles). Occupational exposure was defined as ever exposed to vapor, gas, dust, or fume in expert-selected jobs. Associations were analyzed by adjusted mixed logistic regression. Results The population included 6% with COPD, 48% who had smoked ≥10 pack-years, and 46% with occupational exposure. HMOX1 was genotyped in 4423 participants. The adjusted odds ratio (OR) for the association between HMOX1 long allele and COPD was 1.75 [95% confidence interval (CI) 1.18-2.60]. An interaction was evident between HMOX1 long allele and occupational exposure, OR 2.38 (95% CI 1.04-5.46), versus HMOX1 short/medium without exposure. Analyses were replicated in another cohort, aged 20-44 years, N=1168, including 3% with COPD, 25% who had smoked ≥10 pack-years and 20% with occupational exposure. No associations were seen between COPD and HMOX1 long allele here. Conclusions Long alleles in HMOX1 alone and in interaction with occupational exposure seem to be associated with COPD. Failure to replicate data may be due to premature age for COPD development and low occupational exposure prevalence. We propose this long allele may be a genetic contributor to the COPD pathogenesis.

U2 - 10.5271/sjweh.3846

DO - 10.5271/sjweh.3846

M3 - Journal article

C2 - 31411335

JO - Scandinavian Journal of Work, Environment & Health

JF - Scandinavian Journal of Work, Environment & Health

SN - 0355-3140

ER -