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A 2023 analysis found that U.S. adults in the highest quartile of measured polycyclic aromatic hydrocarbon (PAH) body burden had 2.2 times the adjusted odds of reporting rheumatoid arthritis as adults in the lowest quartile. That is an association with existing, self-reported disease—not evidence that PAHs doubled a person’s chance of developing rheumatoid arthritis in the future.
What the study found
Beidelschies and colleagues analyzed National Health and Nutrition Examination Survey (NHANES) data collected from 2007 through 2016. The cross-sectional study included 21,987 adults: 1,418 classified as having rheumatoid arthritis (RA) and 20,569 who reported no arthritis. RA classification was based on participants reporting that a health professional had told them they had arthritis and then identifying it as rheumatoid arthritis; the analysis did not independently confirm diagnoses.
For the combined measure of PAH body burden, participants in the highest quartile had higher adjusted odds of prevalent, self-reported RA than those in the lowest quartile: odds ratio (OR) 2.2 (95% confidence interval 1.09–4.2; p=0.028). The model adjusted for age, sex, urine creatinine, body mass index, smoking, race, education, family poverty income ratio, physical activity and dietary fibre. The result describes a comparison within this study sample, not a forecast for an individual.
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What “doubled” means—and what it does not
The reported 2.2 is an odds ratio, not a direct measure of risk or incidence. The study compared the odds of having prevalent RA across exposure groups at one point in time; it did not follow people to see who later developed the disease. An odds ratio also is not automatically the same as a risk ratio.
Because exposure and disease were assessed in a cross-sectional analysis, the study cannot establish whether PAH exposure came before RA. It therefore cannot show that PAHs caused rheumatoid arthritis or that reducing exposure would prevent it.
Which PAH result stood out
Researchers assessed PAH metabolites in urine, alongside urine measurements of phthalate and plasticiser metabolites and blood measurements of volatile organic compound (VOC) metabolites. Among individual toxicants, 1-hydroxynaphthalene was the only one reported as remaining associated with RA in the fully adjusted model: highest versus lowest quartile OR 1.8 (95% CI 1.1–3.1; p=0.020). This individual-metabolite finding is distinct from the combined PAH body-burden result.
Phthalate/plasticiser metabolites and VOC metabolites were not associated with RA in the fully adjusted models. These findings do not establish that those substances have no health effects; they describe the associations tested in this analysis.
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The authors’ mediation analysis estimated that PAH body burden accounted for 90% of the total effect of smoking on RA in their statistical model. That percentage is a model-based mediation estimate, not proof of a biological pathway or evidence that PAHs explain 90% of smoking-related RA in people generally.
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After accounting for PAH body burden, the reported smoking association was OR 1.4 (95% CI 0.89–2.3; p=0.13). Because the confidence interval includes 1, this adjusted association was not statistically significant in the reported model. The cross-sectional design cannot determine whether PAH exposure mediates a causal effect of smoking.
Where PAHs can come from
PAHs are a class of chemicals associated with burning coal, oil, gas, wood or tobacco, and with grilling meat, as described in the study. These are possible exposure contexts, not evidence that a particular source caused an individual’s rheumatoid arthritis.
What remains uncertain
- Direction of the relationship: The cross-sectional data cannot establish that exposure preceded disease.
- Disease classification: RA status relied on participant reports rather than objective confirmation within this analysis.
- Exposure measurement: The authors note that biospecimens were limited to blood or urine, which cannot by themselves establish a person’s long-term exposure history.
- Causality: The observed association may be consistent with a possible contribution from combustion-related pollutants, but the study does not prove a causal effect.
Commenting on the findings, Roy Harrison, professor of environmental health at the University of Birmingham, told Chemistry World on 18 May 2023: “There can be no certainty that PAH are the causal factor, if this relationship is indeed causal.” He described combustion-related pollutants as a possible contributory factor, while cautioning that the study does not establish causation.
What readers should take from the finding
The study identifies a statistical association worth investigating further: higher PAH body burden was linked with higher odds of prevalent, self-reported RA in this NHANES sample. It does not establish an individual’s future risk, identify a specific source as responsible, or test whether a product or intervention prevents rheumatoid arthritis.
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