PubMed · 1979374
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Indoor air pollution in developing countries.. https://pubmed.ncbi.nlm.nih.gov/1979374/
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Chloroform (CHCl3) is a short-lived ozone-depleting substance not currently regulated under the Montreal Protocol. Due to the unique meteorological conditions in East Asia, CHCl3 emitted in this region has a greater potential to reach the stratosphere and contribute to ozone depletion. As an essential component of national CHCl3 emissions, southeastern China has attracted increasing attention. However, long-term observational data in this region remain relatively scarce, with no updates since 2020. In this study, we continuously measured atmospheric CHCl3 concentrations at a remote monitoring station in southeastern China from 1 June 2023 to 31 May 2025. Frequent concentration enhancements were observed during the monitoring period, with mixing ratios ranging from 9.3 to 134.1 ppt and an average value of 36.8 ± 19.7 ppt. Back-trajectory analysis indicated that air masses associated with elevated CHCl3 levels primarily originated from coastal industrial provinces in eastern China. Using the Potential Source Contribution Function and Concentration Weighted Trajectory methods, we identified the Yangtze River Delta (Jiangsu, Anhui, and Zhejiang Provinces) and Jiangxi Province as dominant source regions. Emissions of CHCl3 in southeastern China were estimated using the Tracer Ratio Method to be approximately 30.1 ± 5.3 Gg/yr from 2023-06-01 to 2025-05-31, indicating overall stability relative to earlier estimates and no apparent upward trend. These findings provide updated insights into the current status of CHCl3 emissions in southeastern China and highlight the need for continued monitoring and emission assessment of CHCl3 in East Asia, given its unregulated status and implications for ozone layer recovery.
The effects of tropospheric ozone on lung function and respiratory symptoms have been well documented at relatively high concentrations. However, previous investigations have failed to establish a clear association between tropospheric ozone and respiratory diseases severe enough to require hospitalization after controlling for climate, and with gaseous and particulate air pollution at the lower concentrations typically observed in Canada today. To determine if low levels of tropospheric ozone contribute to hospitalization for respiratory disease, air pollution data were compared to hospital admissions for 16 cities across Canada representing 12.6 million people. During the 3927-day period from April 1, 1981, to December 31, 1991, there were 720,519 admissions for which the principle diagnosis was a respiratory disease. After controlling for sulfur dioxide, nitrogen dioxide, carbon monoxide, soiling index, and dew point temperature, the daily high hour concentration of ozone recorded 1 day previous to the date of admission was positively associated with respiratory admissions in the April to December period but not in the winter months. The relative risk for a 30 ppb increase in ozone varied from 1.043 (P < 0.0001) to 1.024 (P = 0.0258) depending on the selection of covariates in the regression model and subset of cities examined. The association between ozone and respiratory hospitalizations varied among cities, with relative risks ranging from 1.000 to 1.088 after simultaneous covariate adjustment. Particulate matter and carbon monoxide were also positively associated with respiratory hospitalizations. These results suggest that ambient air pollution at the relatively low concentrations observed in this study, including tropospheric ozone, is associated with excess admissions to hospital for respiratory diseases in populations experiencing diverse climates and air pollution profiles.
Ozone at ambient concentrations affects lung function and initiates an inflammatory response of the airways. However, the underlying mechanisms are poorly understood. In vitro studies have shown that ozone reacts with water to give reactive hydroxyl radicals capable of oxidizing a wide range of biomolecules. We conducted a study to determine if in vivo hydroxyl radical attack on human airways occurs under natural exposure to ozone. The relation of orthotyrosine to para-tyrosine as a measure of hydroxyl radical attack was analyzed in nasal lavage samples of 44 primary school children in an epidemiologic study. Repeated nasal lavages were performed between May and October 1991 both following "low" (daily half-hour maximum < 140 micrograms/m3, approximately 70 ppb) and "high" (daily half-hour maximum > 180 micrograms/m3, approximately 90 ppb) ozone exposure. Concomitantly, lung function tests were performed. On average, 11.6 (6-16) nasal lavages were performed for each of 24 study days (10 days following "low" ozone exposure and 14 days following "high" ozone exposure). Average ortho-tyrosine (median; 5-95% percentile) for each child was 0.037 mumol/L (0.016-0.064 mumol/L) and average para-tyrosine was 15.7 mumol/L (9.8-24.1 mumol/L). Ortho-tyrosine (as percentage of tyrosine) was significantly higher following days with "high" ozone exposure (0.18%) vs. days following "low" ozone exposure (0.02%; p = .0001). Ortho-tyrosine showed an inverse relationship with forced vital capacity (p = .01) but was not related to inflammation of the upper airways as assessed by cell counts of polymorphonuclear neutrophils. Hydroxyl radical attack subsequent to ambient ozone occurs in the upper airways of healthy children and is related to lung function decrements.