Background: There are few published studies concerning occupational exposure to glyphosate (GLY), and these are limited to spraying, horticulture and other agricultural aspects. Therefore, the concentration of glyphosate and its metabolite aminomethylphosphonic acid (AMPA), in the urine of workers exposed to glyphosate during glyphosate production was determined, and the relationship between internal (urinary glyphosate and AMPA concentration) and external exposure dose (time weighted average (TWA) value of glyphosate in the air of workplace) was analyzed. Methods: To avoid the influence of preparations, we selected people who were only involved in GLY production (without exposure to its preparations) as our research subjects. We collected 134 urine samples of workers exposed to GLY (prototype, not preparation). The urinary concentrations of GLY and AMPA (internal exposure dose) were detected by gas chromatography-mass spectrometry. The subjects’ exposure to the amount of GLY in the air (external dose) was determined using ion chromatography. Conventional statistical methods, including quartiles, t-tests and regression analysis, were applied for data processing. Results: An on-site investigation revealed that the workers involved in centrifugation, crystallization, drying, and packaging and feeding were exposed to GLY. The TWA value of GLY in the workshop air was <0.02 mg/m³–34.58 mg/m³. The detection rates of GLY and AMPA in the urine samples were 86.6% and 81.3%, respectively. The concentration of urinary GLY was <0.020–17.202 mg/L (median, 0.292 mg/L). The urinary AMPA concentration was <0.010 mg/L–2.730 mg/L (median, 0.068 mg/L). The geometric means were 0.262 mg/L and 0.072 mg/L for GLY and AMPA, respectively. There was a correlation between the urinary concentration of GLY and AMPA and the TWA value of exposed workers (correlation coefficient [r] = 0.914 and 0.683, respectively; p < 0.01). Furthermore, there was a correlation between the urinary concentration of GLY and AMPA in the exposure group (r = 0.736, p < 0.01). Conclusions: The urinary concentration of GLY and AMPA of workers was correlated with the TWA value of workers’ exposure, which could reflect the actual exposure of the workers.

With rapid industrial expansion, air pollution’s adverse neurological effects have gained increasing attention. Children face a greater risk of neurological damage because of their higher breathing rates, developing brains, and limited ability to detoxify harmful substances. Fine particulate matter has been identified as a primary neurotoxic contributor affecting developing brains. Strong evidence connects environmental pollutant exposure to the prevalence of Autism Spectrum Disorder (ASD), a neurodevelopmental condition marked by lasting difficulties with social communication and interaction. This study explores the association between long-term PM_2.5 exposure and ASD symptom exacerbation, investigating underlying mechanisms. We hypothesize that long-term PM_2.5 exposure exacerbates ASD symptoms through neuroinflammatory activation, leading to neuronal damage and impaired synaptic plasticity. Our investigation employs three complementary approaches: First, integrated analysis combining Global Burden of Disease data with Mendelian randomization demonstrates a significant association between PM_2.5 exposure and increased ASD severity risk. Second, utilizing the China High-Resolution Air Pollution Database in conjunction with cohort studies, we provide evidence that ambient air pollution substantially influences autism severity, with PM_2.5 identified as the predominant environmental determinant. Third, through network toxicology, single-cell transcriptomics, and animal experimentation, we demonstrate that chronic PM_2.5 exposure exacerbates valproic acid-induced autism-like behaviors in murine models, identifying CTNNB1, PTEN, CCR2, AKT1, and mTOR as potential core mediating genes. Importantly, these findings represent preliminary results. Several potential confounding factors such as co-exposure to other pollutants and socioeconomic variables have not been fully addressed. While our multi-modal approach provides converging lines of evidence, further validation in larger, more diverse populations with refined control of confounders will be essential to establish causality and elucidate mechanisms. Nonetheless, these early insights advance our understanding of PM_2.5-induced neurotoxicity in the context of ASD and offer timely, albeit preliminary, evidence to inform public health policy.