Abstract
Abstract Disclosure: E.L. Silva: None. Z. Wang: None. S. Rifas-Shiman: None. A. Fleisch: None. H. Gibson: None. D. Gold: None. J. Chavarro: None. M. Hivert: None. E. Oken: None. B. Coull: None. J.E. Hart: None. T. James-Todd: None. S. Mahalingaiah: None. Background: The trend towards younger age at menarche over several decades has raised concern as earlier menarche is associated with various adverse health outcomes throughout adulthood including higher risk of early menopause, reproductive cancers, and metabolic disease. Some have suggested environmental exposures early in life may contribute to the temporal trend. Here we aimed to determine the extent to which prenatal residential measures of fine particulate matter (PM2.5), black carbon (BC), and other markers for traffic-related air pollution are associated with earlier age at menarche. Study Methods: Our study population included all female offspring in Project Viva, a pre-birth prospective cohort, with available age at menarche data. We used daily spatiotemporal models to estimate prenatal residential PM2.5 and BC exposures overall and by trimester. Residential proximity to major roadway and traffic density within a 100m buffer were measured at birth. Age at menarche was assessed via questionnaires during pre-teen and teen years. We used Cox proportional hazards modeling, adjusted for sociodemographic variables and census tract median household income, to estimate hazard ratios (HRs) for the association between air pollutants and age at menarche (months), where HR>1 indicates earlier onset of age at menarche associated with increased exposure to air pollutants. We weighted observations by the inverse probability of having available outcome data among all female offspring to account for cohort attrition. Results: The study included 638 females born between 2000 and 2003. Mean (standard deviation (SD)) age at menarche was 12.7 (1.4) years. Mean (SD) prenatal PM2.5 and BC exposures were 11.3 (1.5) g/m3 and 0.72 (0.21) g/m3, respectively. Only 7% of the cohort lived within 100m of a major roadway at birth. Prenatal PM2.5 exposure was not associated with age at menarche and the exposure distribution was mostly below US standards at the time (range: 6.8-15.8 g/m3, interquartile range (IQR): 2.0-3.0 g/m3). Higher overall prenatal and 3rd trimester BC were associated with earlier age at menarche [e.g., HR: 1.26 (95% CI, 1.04, 1.54) per IQR increment in 3rd trimester BC]. Living within 100m of a major roadway (versus 200m) [HR = 1.42 (95% CI, 1.08, 1.86)] and living in areas in the 2nd or 3rd (versus 1st) tertile of traffic density [2nd tertile: HR = 1.37 (95% CI, 1.07, 1.76); 3rd tertile: HR = 1.30 (95% CI, 1.02, 1.66)] at birth were also associated with earlier age at menarche. Conclusions: Higher prenatal exposure to BC, closer residential proximity to road major roadways, and higher traffic density were all associated with earlier age at menarche. The 3rd prenatal trimester and the window around birth may be especially important for traffic-related endocrine-disrupting and pro-inflammatory exposures with potential to accelerate puberty timing among females. Presentation: 6/1/2024
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