Comparison of hospitalization and mortality associated with short-term exposure to ambient ozone and PM2.5 in Canada.

BACKGROUND: Hospitalization and mortality (H-M) have been linked to air pollution separately. However, previous studies have not adequately compared whether air pollution is a stronger risk factor for hospitalization or mortality. This study aimed to investigate differences in H-M risk from short-term ozone and PM2.5 exposures, and determine whether differences are modified by season, age, and sex. METHODS: Daily ozone, PM2.5, temperature, and all-cause H-M counts (ICD-10, A00-R99) were collected for 22-24 Canadian cities for up to 29 years. Generalized additive Poisson models were employed to estimate associations between each pollutant and health outcome, which were compared across season (warm, cold, or year-round), age (all ages or seniors > 65), and sex. RESULTS: Overall, ozone and PM2.5 showed higher season-specific risk of mortality than hospitalization: warm-season ozone: 0.54% (95% credible interval, 0.20, 0.85) vs. 0.14% (0.02, 0.27) per 10 ppb; and year-round PM2.5: 0.90% (0.33, 1.41) vs. 0.29% (0.03, 0.56) per 10 µg/m3. While age showed little H-M difference, sex appeared to be a modifier of H-M risk. While females had higher mortality risk, males had higher hospitalization risk: for females, ozone 0.87% (0.36, 1.35) vs. -0.03% (-0.18, 0.11) and PM2.5 1.19% (0.40, 1.90) vs. 0.19% (-0.10, 0.47); and for males ozone 0.20% (-0.28, 0.65) vs. 0.35% (0.18, 0.51). CONCLUSION: This study found H-M differences attributable to ozone and PM2.5, suggesting that both are stronger risk factors for mortality than hospitalization. In addition, there were clear H-M differences by sex: specifically, females showed higher mortality risk and males showed higher hospitalization risk.

Spontaneously occurring mutations in the cyclobutane pyrimidine dimer photolyase gene cause different sensitivities to ultraviolet-B in rice.

Sensitivity to ultraviolet-B (UVB) radiation (280-320 nm) varies widely among rice cultivars. We previously indicated that UV-resistant rice cultivars are better able to repair cyclobutane pyrimidine dimers (CPDs) through photorepair than are UV-sensitive cultivars. In this paper, we report that UVB sensitivity in rice, in part, is the result of defective CPD photolyase alleles. Surjamkhi (indica) exhibited greater sensitivity to UVB radiation and was more deficient in CPD photorepair ability compared with UV-resistant Sasanishiki (japonica). The deficiency in CPD photorepair in Surjamkhi resulted from changes in two nucleotides at positions 377 and 888 in the photolyase gene, causing alterations of two deduced amino acids at positions 126 and 296 in the photolyase enzyme. A linkage analysis in populations derived from Surjamkhi and Sasanishiki showed that UVB sensitivity is a quantitative inherited trait and that the CPD photolyase locus is tightly linked with a quantitative trait locus that explains a major portion of the genetic variation for this trait. These results suggest that spontaneously occurring mutations in the CPD photolyase gene cause different degrees of sensitivity to UVB in rice, and that the resistance of rice to UVB radiation could be increased by increasing the photolyase function through conventional breeding or bioengineering.