Masanari Watanabe

The effect of ambient air pollutants and Asian dust (AD) on absence from school due to sickness has not been well researched. By conducting a case-crossover study, this study investigated the influence of ambient air pollutants and desert sand dust particles from East Asia on absence from school due to sickness. From November 2016 to July 2018, the daily cases of absence due to sickness were recorded in five elementary schools in Matsue, Japan. During the study period, a total of 16,915 absence cases were recorded, which included 4865 fever cases and 2458 cough cases. The relative risk of overall absence in a 10-μg/m³ increment of PM_2.5 and a 0.1-km⁻¹ of desert sand dust particles from East Asia were found with 1.28 (95%CI: 1.15–1.42) and 2.15 (1.04–4.45) at lag0, respectively. The significant influence of PM_2.5 persisted at lag5 and that of desert sand dust particles at lag2. NO₂ had statistically significant effects at lag2, lag3, and lag4. However, there was no evidence of a positive association of O_x and SO₂ with absence from school. These results suggested that PM_2.5, NO₂, and AD increased the risk of absence due to sickness in schoolchildren.

Experimental and controlled human exposure studies have demonstrated additive effects of ambient particulate matter and ozone on health. A few epidemiological studies have suggested that ambient particulate matter components are important for the combined effects of ambient particulate matter and ozone on health. However, few studies have examined whether ozone changes the effects of ambient particulate matter on pro-inflammatory cytokine production. In this study, the influence of ozone on pro-inflammatory cytokine production in response to ambient particulate matter was evaluated. Ambient particulate matter smaller than 1 μm was collected and the suspension of this particulate matter was bubbled through 0.12 ppm and 0.24 ppm ozone. THP1 cells were stimulated by the solution containing the particulate matter with and without bubbling through ozone at 1 μg/mL. The interleukin-8 concentrations in the supernatants of THP1 cells stimulated by collected particulate matter dissolved in solution were 108.3 ± 24.7 pg/mL without ozone exposure, 165.0 ± 26.1 pg/mL for 0.12 ppm ozone bubbling for 1 min, 175.1 ± 33.1 pg/mL for 0.12 ppm for 5 min, 183.3 ± 17.8 pg/mL for 0.12 ppm for 15 min, 167.8 ± 35.9 pg/mL for 0.24 ppm for 1 min, 209.2 ± 8.4 pg/mL for 0.24 ppm for 5 min, and 209.3 ± 14.3 pg/mL for 0.24 ppm for 15 min. Ozone significantly increased interleukin-8 concentrations compared to those for particulate matter dissolved in solution without ozone exposure and the solvent only (8.2 ± 0.9 pg/mL) in an ozone concentration-dependent manner. Collected particulate matter in solutions with or without bubbling through ozone had no effect on interleukin-6 production. The antioxidant N-acetyl-L-cysteine significantly inhibited the increases in interleukin-8 induced by solutions with particulate matter, regardless of ozone exposure. The reactive oxygen species concentration in solutions with collected particulate matter was not associated with ozone bubbling. Ozone may augment the production of interleukin-8 in response to ambient particulate matter by a mechanism unrelated to reactive oxygen species. These results support the epidemiological evidence for combined effects of ambient particulate matter and ozone on human health.