**Background:** Air pollution is a major global public health risk factor, linked to cardiovascular, respiratory, renal, and neurological diseases. Particulate matter and gaseous pollutants are known to induce systemic inflammatory responses, leading to redistribution of peripheral white blood cells (WBCs). However, prior studies on the association between short-term air pollution exposure and WBC counts have yielded inconsistent results, possibly due to differences in study populations, sample sizes, and confounding factors. This study aimed to investigate the association between short-term air pollution exposure and peripheral blood leukocyte distribution in adult males, and to explore the potential influence of air-pollution-induced inflammation.
**Methods:** The study population consisted of 11,035 men aged 22–45 years who visited Peking University Third Hospital Medical Center from January 2015 to December 2019. Individuals with systemic diseases (liver, renal, cardiovascular, hematological, endocrine disorders), infections, inflammation, or abnormal clinical laboratory indicators were excluded. Peripheral blood samples were collected via venipuncture with EDTA-K2 anticoagulant, and leukocytes were counted and classified into five subtypes (neutrophils, eosinophils, basophils, lymphocytes, monocytes) using an SYSMEX XN-2000 automated hematology analyzer. Air pollution data (PM2.5, PM10, SO2, CO, NO2, O3) were obtained from the China Meteorological Administration and Environmental Monitoring Center as 24-hour averages. Meteorological data (temperature, humidity, wind speed, air pressure) were collected from the China Meteorological Data Service Centre. Statistical analysis employed generalized additive models (GAM) with adjustment for age, temperature, humidity, wind speed, air pressure, and season (heating vs. non-heating). Single-day lag effects (lag 0 to lag 3) and moving average lag effects (0–1, 0–2, 0–3 days) were assessed. Results were expressed as percent changes with 95% confidence intervals (CIs).
**Key Results:** The mean age of participants was 30.38 years. Mean peripheral blood counts were: total WBC 6.77 ×10⁹/L, neutrophils 3.94 ×10⁹/L, eosinophils 0.03 ×10⁹/L, basophils 0.13 ×10⁹/L, lymphocytes 2.21 ×10⁹/L, and monocytes 0.36 ×10⁹/L. Mean daily pollutant concentrations were: PM2.5 59.9 μg/m³, PM10 84.42 μg/m³, SO2 8.064 μg/m³, CO 0.99 mg/m³, NO2 43.68 μg/m³, and O3 96.86 μg/m³. Short-term air pollution exposure (0–3 day lag) showed no significant association with total WBC count for any pollutant (p > 0.05). For neutrophils, only PM10 at 2-day lag showed a significant positive association (0.0089% increase per unit; 95% CI: 0.0001–0.0177%). Eosinophils were significantly negatively correlated with PM2.5, PM10, SO2, and CO; the strongest single-day effect was at lag 0 (PM2.5: −0.050%; PM10: −0.028%; SO2: −0.24%; CO: −3.485%; all p < 0.05), and the strongest average lag effect was at 0–2 days (PM2.5: −0.066%; PM10: −0.040%; SO2: −0.309%; CO: −4.633%; all p < 0.05). Basophils were significantly negatively correlated with all six pollutants; the strongest average lag effect was at 0–3 days (PM2.5: −0.136%; PM10: −0.066%; SO2: −1.300%; CO: −8.559%; NO2: −0.204%; O3: −0.099%; all p < 0.05). Lymphocytes were significantly positively associated only with PM2.5 (0.012% increase per unit; p < 0.05). Monocytes were significantly positively associated with NO2 (0.043% increase per unit at 0–3 day average; p < 0.05) and significantly negatively associated with O3 (−0.031% per unit at 0–3 day average; p < 0.05).
**Clinical Implications:** This study demonstrates that short-term exposure to both particulate and gaseous air pollutants significantly alters peripheral blood leukocyte distribution in adult males, with a pattern suggesting systemic inflammation (increased neutrophils, lymphocytes, monocytes) and potential bone marrow suppression (decreased eosinophils, basophils). These changes may represent an early inflammatory response that could contribute to the pathogenesis of air-pollution-related diseases, including cardiovascular disease and male infertility. The findings highlight the need for longer-term studies (weeks to months) to assess cumulative effects. Limitations include the use of area-level rather than individual-level pollution exposure data, lack of indoor/outdoor activity data, and the absence of other inflammatory markers such as C-reactive protein (CRP) and cytokines. The study's strengths include a large sample size, adjustment for multiple meteorological and seasonal confounders, and assessment of both single-day and moving-average lag effects across multiple pollutants.