Low Exposure to Secondhand Smoke Is Linked to a Rheumatoid Arthritis Risk

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When the serum cotinine levels were below -2.756 ng/mL, each 1 ng/mL increase in log-2-transformed serum cotinine levels increased the RA risk by 16.3%.

Low Exposure to Secondhand Smoke Is Linked to a Rheumatoid Arthritis Risk

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A new study revealed low exposure to secondhand smoke is linked to rheumatoid arthritis (RA) risk—but not moderate or high exposure.1

Secondhand smoke was responsible for approximately 1.3 million deaths worldwide in 2019 alone.2 Already, research found secondhand smoke is associated with increased risks of cancer, cardiovascular diseases, respiratory diseases, type 2 diabetes, and osteoporosis.1 However, despite smoking being a recognized factor for RA, research on the link between secondhand smoke and RA in non-smoking adults was limited.

Investigators, led by Xiaogang Qui, from the department of orthopedics at the Second Hospital of Shanxi Medical University in China, aimed to evaluate this association using serum cotinine levels.

“The NHANES presents a unique opportunity to investigate the potential association between [secondhand smoke] exposure and RA, as well as the dose-response relationship between the two,” investigators wrote. “In contrast to previous studies, our research took a dual approach. We used self-reported criteria to identify non-smokers and employed serum cotinine levels to quantify [secondhand smoke] exposure.”

Conducting a cross-sectional study, Qui and colleagues leveraged data from the National Health and Nutrition Examination Survey from 1999 – 2018. They included 14,940 adults who self-reported as never smokers in their analysis, focusing on respondents aged ≥ 20 years old. Participants were excluded if they were pregnant or had missing data on RA, serum, cotinine, and other covariates.

Never smokers were defined as participants who reported having ≤ 100 cigarettes in their lifetime and did not consume any nicotine products in the past 5 years. Participants were considered former smokers if they had a history of smoking ≥ 100 cigarettes but were not currently smoking. Current smokers smoked ≥ 100 cigarettes in their lives, were actively smoking during the study, and had many had serum cotinine levels ≥ 10 ng/mL.

Secondhand smoke was broken into 4 groups based on serum cotinine levels: unexposed (serum cotinine < 0.05 ng/mL), low exposure (serum cotinine at 0.05 to 0.99 ng/mL), moderate exposure (serum cotinine at 1 to 10 ng/mL), or the heavy exposure group (serum cotinine ≥ 10 ng/mL).

Investigators adjusted for the covariates of age, gender, marital status, race/ethnicity (non-Hispanic white, non-Hispanic black, Mexican American, other), educational level (< 9 years, 9 – 12 years, ≥ 12 years), family income (poverty income ratio grouped as low ≤ 1.3, medium > 1.3 and ≤ 3.5, and high > 3.5), hypertension, diabetes, coronary heart disease, body mass index, physical activity (sedentary, moderate, vigorous), alcohol user (never, former, mild, moderate, heavy), fish intake (within past 30 days), and asthma.

The sample had an average age of 46.7 ± 17.6 years, with 60.2% female and 39.7% identifying as non-Hispanic White. Participants with RA tended to be older, living alone, having a lower educational level and family income, and experiencing a greater incidence of hypertension and diabetes.

Compared to the unexposed group, the low exposure group had 1.37 odds for developing RA (adjusted odds ratio [aOR], 1.37; 95% CI, 1.14 – 1.64; P = .0001). However, the moderate or heavy exposure groups had no significant association with RA.

The team observed a non-linear, positively saturated correlation between the cotinine levels after log2 transformation and RA (P = .028). They saw a turning point at about 2.756 ng/mL (OR, 1.163; 95% CI, 1.073 – 1.261, P = .0002). A subgroup analysis confirmed the finding.

“When the log2-transformed serum cotinine levels were below − 2.756 ng/mL, each 1 ng/mL increase in log2-transformed serum cotinine levels corresponded to a 16.3% increase in the risk of developing RA,” investigators wrote. “However, no significant correlation was found between SHS exposure and RA risk when the log2-transformed serum cotinine levels were exceeded − 2.756 ng/mL.”

The results indicate low exposure to secondhand smoke increases the risk of developing RA with a saturation effect.

The team wrote how the results were limited by the fact there is no universally accepted biomarker to distinguish between thirdhand smoke and secondhand smoke exposure—and thirdhand smoke exposure can also affect serum cotinine levels. Thus, biases may exist when using serum cotinine levels to evaluate secondhand smoke exposure.

Other limitations investigators highlighted included the cross-sectional design, the short half-life of serum cotinine preventing the ability to assess long-term secondhand smoke exposure, and the large timeline potentially impacting the results due to temporal bias.

“These findings aim to capture the attention of non-smokers,” investigators concluded. “Moreover, further large-scale prospective investigations are necessary to confirm and extend our findings.”

References

  1. Qi X, Fu J, Liu J, Wu X, Zheng X, Wang S. Association between secondhand smoke exposure and rheumatoid arthritis in US never-smoking adults: a cross-sectional study from NHANES. Sci Rep. 2024;14(1):11061. Published 2024 May 14. doi:10.1038/s41598-024-61950-2
  2. Zhai C, Hu D, Yu G, et al. Global, regional, and national deaths, disability-adjusted life years, years lived with disability, and years of life lost for the global disease burden attributable to second-hand smoke, 1990-2019: A systematic analysis for the Global Burden of Disease Study. Sci Total Environ. 2023;862:160677. doi:10.1016/j.scitotenv.2022.160677
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