PubMed · 697974
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J D Shannon, M L Wesely. 1978. Objective sensor placement for sampling regional turbidity.. https://doi.org/10.1016/0004-6981(78)90033-1
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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.
BACKGROUND: Most public-health assessments of climate-control policies have focused on long-term impacts of global change. Our interdisciplinary working group assesses likely short-term impacts on public health. METHODS: We combined models of energy consumption, carbon emissions, and associated atmospheric particulate-matter (PM) concentration under two different forecasts: business-as-usual (BAU); and a hypothetical climate-policy scenario, where developed and developing countries undertake significant reductions in carbon emissions. FINDINGS: We predict that by 2020, 700,000 avoidable deaths (90% CI 385,000-1,034,000) will occur annually as a result of additional PM exposure under the BAU forecasts when compared with the climate-policy scenario. From 2000 to 2020, the cumulative impact on public health related to the difference in PM exposure could total 8 million deaths globally (90% CI 4.4-11.9 million). In the USA alone, the avoidable number of annual deaths from PM exposure in 2020 (without climate-change-control policy) would equal in magnitude deaths associated with human immunodeficiency diseases or all liver diseases in 1995. INTERPRETATION: The mortality estimates are indicative of the magnitude of the likely health benefits of the climate-policy scenario examined and are not precise predictions of avoidable deaths. While characterized by considerable uncertainty, the short-term public-health impacts of reduced PM exposures associated with greenhouse-gas reductions are likely to be substantial even under the most conservative set of assumptions.
The genotoxic risks from exposure to polycyclic aromatic hydrocarbons (PAH) have long been recognized. Less well understood are the potential genotoxic risks of the atmospheric reaction products of this class of compounds. In this investigation, we have utilized several human cell genotoxicity assays to evaluate naphthalene, phenanthrene, and their atmospheric reaction products 1-nitronaphthalene, 2-nitronaphthalene, 1-hydroxy-2-nitronaphthalene, 2-hydroxy-1-nitronaphthalene, 1,4-naphthoquinone and 2-nitrodibenzopyranone. In addition, reaction products of naphthalene were generated in a 6700-1 Teflon environmental chamber, collected on a solid adsorbent, extracted and fractionated by normal-phase HPLC. Individual fractions were then analyzed using GC-MS, and tested for genotoxicity. Genotoxicity was determined using the human B-lymphoblastoid cell line, MCL-5, which expresses several transfected P450 and epoxide hydrolase genes. Mutagenicity was evaluated at both the heterozygous tk locus and the hemizygous hprt locus, permitting detection of both intragenic and chromosomal scale mutational events. Test compounds were also screened using the CREST modified micronucleus assay. Genotoxicity results indicate that 2-nitronaphthalene and 2-nitrodibenzopyranone possess greater mutagenic potency than their parent compounds, and interestingly, both compounds induced significant increases in mutation frequency at tk but not hprt. These results suggest a mechanistic difference in human cell response as compared to bacteria, where both compounds were previously shown to induce point mutations in the Salmonella reversion assay. The genotoxicity of 2-nitronaphthalene and 2-nitrodibenzopyranone in human cells, together with their high concentrations in ambient air relative to nitro-PAH directly emitted from combustion sources, emphasizes the need to consider atmospheric reaction products of PAH in genotoxicity assessments.