Risk of developing rheumatoid arthritis doubled by polycyclic aromatic hydrocarbons exposure

Exposure to polycyclic aromatic hydrocarbons (PAHs), which form during combustion, could significantly increase an individual’s risk of developing rheumatoid arthritis (RA), regardless of whether they smoke or not. The authors said the findings confirmed, and expanded on, the limited evidence for the relationship between PAHs and RA.

PAHs are a class of ubiquitous chemicals formed when coal, oil, gas and wood are burnt or through the grilling of meat. Tobacco is also a known source of PAHs.

The cross-sectional study aimed to explore the association between PAHs in smokers and non-smokers, and RA prevalence while controlling for important confounders such as age, sex and body mass index. It included over 21,000 adult participants, 1418 of which had RA, using data collected between 2007 and 2016 by the US National Health and Nutrition Examination Survey.

Associations between individual toxicants – including phthalate and plasticiser metabolites or volatile organic compounds (VOCs), as well as PAHs – and RA were assessed. A body burden score was established for each participant, via blood and urine samples, which provided a measure of their exposure to these chemicals via the resulting metabolites.

When comparing those in the highest quartile for PAH body burden with those in the lowest quartile, the odds of developing RA were more than doubled. After adjusting for confounding factors, only one PAH, 1-hydroxynaphthalene, was associated with increased odds of developing RA. In contrast, phthalate, plasticiser and VOC metabolites were not associated with RA in fully adjusted models.

The researchers also analysed whether PAH body burden mediated the relationship between smoking and RA. They found that smoking was associated with RA, as well PAH body burden and PAH body burden was still associated with RA after adjusting for smoking. From this, the authors calculated that PAH body burden mediated almost 90% of the total effect of smoking on RA. PAH body burden was also significantly associated with RA in non-smokers but did not achieve significance in the fully-adjusted model.

The authors said that, to their knowledge, theirs was the first study to demonstrate that PAHs not only underlie the majority of the relationship between smoking and RA, but also independently contribute to RA.

‘The current study supports and expands the available evidence demonstrating that environmental PAHs are associated with RA prevalence in the US population, regardless of smoking status,’ the authors write.

Roy Harrison, professor of environmental health at the University of Birmingham, says that while the study was ‘carefully conducted’ it was important not to ‘over-interpret’ the findings. ‘The results show several positive and statistically significant positive associations between self-reported rheumatoid arthritis and several PAH metabolites measured in urine,’ he adds. ‘Such associations were not found with phthalate plasticisers or toluene.’

Harrison adds that the limitations of the study included the lack of an objective determination of disease or diagnosis and the small effect sizes for individual metabolites. ‘My interpretation is that the study supports the likelihood that exposure to combustion-related pollutants is a contributory factor in rheumatoid arthritis.

‘There can be no certainty that PAH are the causal factor, if this relationship is indeed causal,’ Harrison explains. ‘However, the results suggest that top quartile exposures lead to a doubling of disease risk relative to lowest quartile exposures, which is important in public health terms.’