Ambient Air Pollution, Polycyclic Aromatic Hydrocarbons, and Pubertal Development: A Critical Review of Emerging Evidence

Ambient aromatic hydrocarbons and prostate cancer: mechanistic evidence linking benzene and PAH exposure to tumor progression

Current evidence supports a biologically plausible framework in which AH exposure may contribute to PCa initiation and progression and may intersect with pathways implicated in therapy resistance, although causal inference remains constrained by exposure misclassification, mixture complexity, and limited longitudinal biomarker data.

Prenatal Internal Exposure to Polycyclic Aromatic Hydrocarbons, Maternal Genetic Susceptibility, and Child Growth Trajectories: Evidence from a Prospective Cohort Study

Prenatal exposure to polycyclic aromatic hydrocarbons (PAHs) is a widespread environmental health concern, yet its impact on early childhood growth trajectories remains poorly understood. In a prospective birth cohort in China (PKUBC-T), we identified distinct growth trajectories from birth to age 3 years using K-means clustering for longitudinal data (N = 1467) and measured 16 plasma PAHs in first-trimester maternal samples (N = 333). Twenty maternal single nucleotide polymorphisms (SNPs) related to PAHs metabolism were genotyped. Modified Poisson and weighted quantile sum regression showed that higher prenatal PAHs exposure was associated with increased risk of rapid higher growth trajectory, with phenanthrene, pyrene, and fluoranthene contributing most. This trajectory is characterized by a marginally higher BMI Z-score at birth, followed by rapid growth during infancy and sustained high levels thereafter. Furthermore, the AHR rs2066853 variant significantly modified the association, with the positive association being observed only among mothers carrying GA/AA genotypes (RR, 2.44; 95% CI, 1.51–3.97) but not among those with GG homozygotes (P for interaction is 0.049). We provide evidence that prenatal PAHs exposure may alter early childhood growth patterns, with effects modified by maternal genetic susceptibility. If confirmed, these findings highlight the mechanistic importance of AHR signaling in environmental developmental toxicity and underscore the need for exposure reduction and targeted maternal monitoring.

Association of prenatal exposure to PM2.5 and its chemical constituents with early childhood obesity: A population-based study.

A growing body of evidence links gestational fine particulate matter (PM2.5) exposure to elevated childhood obesity risk, yet research on the combined impacts and respective contributions of different PM2.5 chemical constituents remains limited. This large population-based prospective study involved 339,435 mother-child pairs from Liaoning Province, China. Prenatal exposure to PM2.5 and five major chemical constituents (organic matter (OM), black carbon (BC), ammonium (NH₄⁺), nitrate (NO₃⁻), sulfate (SO₄²⁻)) was estimated using high-resolution atmospheric reanalysis data. Quantile g-computation (QGC) was used to investigate the joint associations of PM2.5 chemical constituent mixtures and the relative contribution of each constituent with childhood overweight/obesity (OwOb) risk across the first two years of life. In single-pollutant models, prenatal exposure to PM2.5 total mass (per interquartile range, odds ratio (OR) = 1.050, 95% confidence interval (CI): 1.036, 1.064) and four of the five chemical constituents (OM: OR = 1.058, 95% CI: 1.043, 1.072; NH₄⁺: OR = 1.048, 95% CI: 1.035, 1.062; NO₃⁻: OR = 1.048, 95% CI: 1.033, 1.064; and BC: OR = 1.033, 95% CI: 1.020, 1.047) were positively associated with increased risks of offspring OwOb. A one-quartile increase in the mixture of multiple PM2.5 chemical constituents was associated with increased OwOb risk (OR = 1.063, 95% CI: 1.050, 1.076), with OM (54.1%), NH₄⁺ (34.4%), and NO₃⁻ (11.5%) acting as major contributors to the overall mixture effects. These findings underscore that regulating key PM2.5 chemical constituents is a vital public health strategy to mitigate the adverse effects of prenatal air pollution on children's metabolic health.

A Cross-Sectional Study on Immune-Inflammatory Responses: Exposure to Polycyclic Aromatic Hydrocarbons Alters Pteridine Metabolism and Activates the Kynurenine Pathway

Polycyclic aromatic hydrocarbons (PAHs) are common environmental pollutants generated from the incomplete combustion of organic materials and represent an important source of occupational and environmental exposure. Aside from their carcinogenic properties, PAHs are known to exert immunomodulatory and proinflammatory effects. Immune activation is closely associated with alterations in pteridine metabolism and activation of the kynurenine pathway; however, evidence linking PAH exposure to these immune-inflammatory pathways in humans remains limited. This study aimed to investigate the systemic biological effects of occupational exposure to PAHs from asphalt fumes in road construction workers, with a particular focus on alterations in pteridine metabolism and activation of the kynurenine pathway, using a combined panel of exposure and mechanistic biomarkers. Routine clinical parameters remained within normal ranges while urinary 1-hydroxypyrene, a well-established biomarker of internal PAH exposure, was significantly elevated, confirming substantial PAH exposure. Key findings revealed profound alterations in two critical metabolic pathways: (i) Pteridine metabolism was shifted, with increased neopterin and decreased biopterin levels, indicating activation of cell-mediated immunity and reduced cofactor availability; (ii) the kynurenine pathway was concurrently activated, as reflected by elevated kynurenine, reduced tryptophan, and increased estimated indoleamine 2,3-dioxygenase activity. These findings indicate that low-level but chronic PAH exposure induces sustained Th1-type immune activation and metabolic disturbances in the absence of overt clinical pathology, representing a state of subclinical biological adaptation.

Long-Term PM2.5 Exposure and Timing of Pubertal Development in Boys and Girls: A Prospective Cohort Study in Chongqing, China.

BACKGROUND PM2.5, a ubiquitous air pollutant with endocrine-disrupting potential, may contribute to the global trend of earlier puberty, yet evidence remains limited to isolated milestones and largely excludes boys. METHODS We analyzed 3,833 children from the Chongqing Child Health Cohort (2014-2024). Time-varying PM2.5 exposure was defined as cumulative average residential PM2.5 from the prenatal period to milestone onset or censoring. Cox models were used to examine associations between cumulative average PM2.5 exposure and the timing of multiple pubertal milestones, with stratification by weight status and underlying health conditions and evaluation of whether these associations varied according to long-term average temperature and relative humidity. RESULTS In girls, each 1 μg/m3 increase in cumulative average PM2.5 exposure was associated with earlier breast development (HR = 1.044, 95% CI: 1.039-1.050), pubic hair (HR = 1.038, 95% CI: 1.032-1.045) and menarche (HR = 1.033, 95% CI: 1.025-1.040), with a weaker association for axillary hair development (HR = 1.012, 95% CI: 1.005-1.020). In boys, each 1 μg/m3 increase was associated with earlier testicular development (HR = 1.065, 95% CI: 1.056-1.073), penile development (HR = 1.063, 95% CI: 1.055-1.071), pubic hair (HR = 1.032, 95% CI: 1.022-1.041), and beard development (HR = 1.032, 95% CI: 1.023-1.041), with a weaker association for spermatorrhea (HR = 1.024, 95% CI: 1.003-1.046). Associations varied by weight status and according to long-term average temperature and relative humidity, with stronger associations for several milestones among overweight/obese girls and stronger associations overall in areas with higher long-term average temperatures and lower long-term relative humidity. CONCLUSION Long-term PM2.5 exposure is associated with earlier onset of secondary sexual characteristics and key reproductive milestones across the pubertal trajectory. The observed associations varied according to long-term average temperature, relative humidity, and weight status, suggesting heterogeneity according to both background environmental conditions and individual susceptibility.

Prenatal exposure to environmental toxicants and their association with alterations in kidney development.