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0231  Acute inflammatory response to secondhand smoke exposure among non-smoking construction workers: a repeated measures study0231  Acute inflammatory response to secondhand smoke exposure among non-smoking construction workers: a repeated measures study
  1. Jennifer Bruno Garza1,
  2. Jinming Zhang2,
  3. Shona Fang2,
  4. Jason Wong2,
  5. David Christiani2,
  6. Jennifer Cavallari1
  1. 1University of Connecticut Health Center, Farmington, CT, USA
  2. 2Harvard School of Public Health, Boston, MA, USA

Abstract

Objectives This study aimed to characterise the cardiovascular inflammatory response to secondhand smoke (SHS) exposure among non-smoking construction workers.

Method Non-smoking workers (n = 27) were recruited from a local union and monitored inside a union hall while exposed to SHS over approximately 6 h. Using a repeated measures study design, blood samples were taken before SHS exposure (baseline), immediately following SHS exposure (post) and the morning following SHS exposure (next morning). Inflammatory markers including acute phase proteins (SAA, CRP), adhesion molecules (s-ICAM, s-VCAM), and inflammatory cytokines (IL-1, IL-2, IL-6, IL-8, IL-10, TNF-alpha, VEGF) were analysed. Linear mixed effects regression models were used to examine within-person changes in inflammatory markers at post and next morning compared to baseline. Exposure-response relationships with TWA PM2.5 were also examined using mixed effects models. All models were adjusted for age, BMI and circadian variation.

Results There was a decrease in SAA (baseline = 2322 ng/ml, post = 1949 ng/ml, p = 0.04) and TNF-alpha (baseline = 9.6 pg/ml, post = 8.4 pg/ml, p < 0.01) post exposure, as compared to baseline. There was a decrease in IL-10 (baseline = 5.9 pg/ml, next morning = 6.5 pg/ml, p < 0.01) next morning compared to baseline. Increases in SHS-related PM2.5 exposures were associated with significant (p < 0.01) increases in next morning CRP, s-ICAM, and s-VCAM levels.

Conclusions Our results indicate that exposure to SHS can lead to a cardiovascular inflammatory response approximately 18 h following SHS exposures, further supporting a pathway between SHS exposure and adverse cardiovascular outcomes.

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