Airborne occupational exposure, ABO phenotype, and risk of obesity

Our plain-English summary of Airborne occupational exposure, ABO phenotype, and risk of obesity, by P. Suadicani, H.O. Hein, F. Gyntelberg (International Journal of Obesity, 2005).

The study

• Authors: P. Suadicani, H.O. Hein, F. Gyntelberg
• Journal: International Journal of Obesity
• Published: 2005;29(6):689-96
• Cited by: 12 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Background: We have previously found a quite strong interplay between occupational airborne pollutants, ABO phenotypes, and risk of ischaemic heart disease (IHD), with long-term exposure being associated with a significantly increased risk among men with phenotype O, and not among men with other ABO phenotypes. We suggested that the biological pathway could be a stronger systemic inflammatory response in men with blood group O. Several inflammatory mediators likely to increase the risk of IHD have recently been linked also to obesity, suggesting that long-term exposure to airborne pollutants might play a role in the aetiology of obesity. Accordingly, we tested the hypothesis that long-term occupational exposure to airborne pollutants would be more strongly associated with obesity in men with phenotype O than in men with other ABO phenotypes.

Design: Cross-sectional exposure-response study taking into account potential confounders.

Setting: The Copenhagen Male Study.

Subjects: A total of 3290 men aged 53-74 y.

Main Outcome Measure: Prevalence of obesity (BMI > or =30 (kg/m2)).

Results: Overall, no differences were found in the prevalence of obesity between men with the O phenotype (n=1399) and men with other phenotypes (n=1891), 8.6 and 9.0%. However, only among men with the O phenotype was long-term occupational exposure (at least 5 y of frequent exposure) to various respirable airborne pollutants: dust, asbestos, soldering fumes, welding fumes, organic solvents, fumes from lacquer, paint or varnish, toxic components, breath irritants, stench or strongly smelling products, and irritants (other than breath irritants or contagious components) associated with an increased prevalence of obesity. Statistically, the strongest univariate associations were found for asbestos exposure, welding fumes, and breath irritants. Odds ratios (95% confidence limits) for these factors were 3.7 (1.8-7.6), 2.7 (1.6-4.4), and 2.6 (1.5-4.4), respectively. This particular relationship of airborne exposures with obesity in men with phenotype O was supported in multivariate analysis including interaction terms and taking into account a number of potential confounders. In contrast, no gene-environment interactions with obesity were found with respect to ABO phenotypes and a number of nonrespirable exposures.

Conclusion: The finding of a quite strong interplay between long-term exposure to airborne pollutants, ABO phenotypes, and risk of obesity may open up new possibilities for clarifying mechanisms underlying the global obesity epidemic.

In plain English

This cross-sectional study used Copenhagen Male Study data on 3290 Danish men aged 53 to 74, examined in 1985–86. The authors tested whether long-term workplace airborne exposures were more strongly linked to obesity (body mass index 30 or more) in men with blood group O than in other men. Long-term meant self-reported frequent exposure for at least 5 years. Asbestos exposure was reported by 3.4%; no fiber type was specified. Obesity was about as common in group O men (8.6%) as in other men (9.0%). Among group O men, long-term asbestos exposure was linked to higher odds of obesity: odds ratios 3.7 (95% confidence limits 1.8–7.6) unadjusted, 2.4 (1.0–5.9) fully adjusted. Among other men, asbestos odds ratios of 1.6 (0.8–3.4) unadjusted and 1.3 (0.6–3.0) fully adjusted were not statistically significant. After adjustment, group O men reporting 7 to 10 long-term respirable exposures (n=23) had an odds ratio of 8.3 (3.1–22.0) versus group O men reporting none. The authors noted exposures were self-reported and the asbestos finding may be spurious. They concluded this apparent gene–environment interaction may help clarify mechanisms behind the global obesity epidemic.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Cross-sectional exposure–response study within an existing cohort (the Copenhagen Male Study), using logistic regression with adjustment for potential confounders
• Who was studied: 3290 Danish men aged 53–74 years from the Copenhagen Male Study, examined in 1985–86. They were survivors of a 1970–71 cohort of 5249 men; 3387 took part and 97 were excluded for missing values. Men were grouped as blood group O (n=1399) or other ABO phenotypes (n=1891).
• Exposure: Self-reported occupational exposures from a questionnaire. Long-term exposure meant exposure several times a week or more for at least 5 years. There were 10 respirable airborne exposures, including asbestos (reported by 3.4% of the cohort; 3.2% of group O and 3.6% of other men), dust, soldering fumes, welding fumes and organic solvents, plus 12 nonrespirable exposures. No asbestos fiber type was specified.
• Main results:
  • The authors found no overall difference in obesity prevalence between men with blood group O (8.6%) and men with other phenotypes (9.0%).
  • Among men with blood group O, long-term asbestos exposure was associated with obesity at the following odds ratios (95% confidence limits): 3.7 (1.8–7.6) unadjusted; 2.7 (1.2–6.1) adjusted for nonrespirable exposures; 2.4 (1.0–5.9) further adjusted for smoking, alcohol, leisure-time physical activity, social class and age. Asbestos was among the strongest unadjusted associations, along with welding fumes 2.7 (1.6–4.4) and breath irritants 2.6 (1.5–4.4).
  • Among men with blood group O, all long-term airborne exposures remained associated with increased odds of obesity in the fully adjusted model. The association was statistically significant for four of the 10 respirable exposures.
  • Among men with other ABO phenotypes, no association between respirable exposures and obesity was significant at the 0.05 level. For asbestos the odds ratios were 1.6 (0.8–3.4) unadjusted, 1.3 (0.6–2.8) adjusted for nonrespirable exposures, and 1.3 (0.6–3.0) fully adjusted.
  • In a multivariable-adjusted backward elimination model among men with blood group O, those with 7 to 10 long-term respirable exposures (n=23) had an odds ratio for obesity of 8.3 (95% confidence limits 3.1–22.0) compared with unexposed group O men (n=957). Among other men with 7 to 10 exposures (n=23), the odds ratio was 0.8 (0.2–3.4).
  • In an analysis of all men, the interaction between blood group (O versus non-O) and number of respirable exposures was statistically significant (P = 0.003).
• The authors' conclusion: The authors concluded that the findings support men with blood group O being more susceptible, with respect to obesity, to airborne occupational exposures. They said this apparent gene–environment interaction may open up new possibilities for clarifying mechanisms underlying the global obesity epidemic.
• Limitations the authors state:
  • Occupational exposures were based only on self-report, which the authors note can be imprecise. They argued such imprecision would tend to dilute rather than create the associations.
  • The authors stated that the asbestos finding, the strongest point estimate, may be spurious.

Topics

Medical terms in this study, explained in our Lexicon: Occupational Exposure, Asbestos Exposure, Odds Ratio, Multivariate Analysis.

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