Atmospheric pollutants increase the risk of acute ischemic stroke (AIS) which has been widely reported. However, little is known about the relationships between air pollution and specific subsets of AIS, such as wake-up stroke (WUS) and non-wake-up stroke (non-WUS). This study aimed to explore the relationship between WUS and non-WUS and atmospheric pollutants. A total of 1432 patients (331 WUS patients and 1101 non-WUS patients) were admitted to a tertiary hospital from 2016 to 2019. A time-stratified case-crossover design and a conditional logistic regression model to study the associations of change in pollutant concentration with WUS and non-WUS events were constructed. Data analysis revealed that WUS-related risks increased 48 to 72 h after the increase in the PM concentration (each 10 μg/m increase, lag 0-72 h) [threshold OR (95% CI):18 μg/m 1.03 (0.94-1.11), 35 μg/m 1.01 (0.92-1.12), 50 μg/m 1.04 (0.91-1.19)]; the non-WUS-related risk increased 1 to 6 h after the increase in the PM concentration (each 10 μg/m increase, lag 0-1 h) [threshold OR (95% CI):18 μg/m 1.01 (0.98-1.03), 35 μg/m 1.00 (0.97-1.04), 50 μg/m 1.01 (0.96-1.05)] (lag 0-6 h) [threshold OR (95% CI): 18 μg/m 1.00 (0.97-1.03), 35 μg/m 1.00 (0.97-1.04), 50 μg/m 1.01 (0.97-1.06)]; O exposure was related to WUS events, and its impact on WUS events was stronger and longer-lasting (1-96 h) than its impact on non-WUS events (1-6 h). Greater than or equal to 65 years of age, overweight (BMI ≥ 25), and diabetes had a significantly greater risk of WUS associated with increased PM concentration in the previous 12-96 h than patients without these conditions. Patients with hypertension and smoking had a significant risk of non-WUS associated with increased PM concentration in the previous 1-6 h. The increase in PM concentration in the cold season increased the risk of both WUS and non-WUS events. Ambient air pollution hysteresis triggers WUS and rapidly triggers non-WUS, even if the degree of pollutant is relatively low. Patients with elderly, overweight, and diabetes appeared particularly susceptible to WUS, and patients with hypertension and smoking history were susceptible to non-WUS. We need to expand the sample for further investigation into mechanisms by which environmental pollutants trigger WUS or non-WUS.