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Narrowing feedstock exemptions under the Montreal Protocol has multiple environmental benefits.

ABSTRACT: The Montreal Protocol on Substances that Deplete the Ozone Layer (Montreal Protocol) can be further strengthened to control ozone-depleting substances and hydrofluorocarbons used as feedstocks to provide additional protection of the stratospheric ozone layer and the climate system while also mitigating plastics pollution. The feedstock exemptions were premised on the assumption that feedstocks presented an insignificant threat to the environment; experience has shown that this is incorrect. Through its adjustment procedures, the Montreal Protocol can narrow the scope of feedstock exemptions to reduce inadvertent and unauthorized emissions while continuing to exempt production of feedstocks for time-limited, essential uses. This upstream approach can be an effective and efficient complement to other efforts to reduce plastic pollution. Existing mechanisms in the Montreal Protocol such as the Assessment Panels and national implementation strategies can guide the choice of environmentally superior substitutes for feedstock-derived plastics. This paper provides a framework for policy makers, industries, and civil society to consider how stronger actions under the Montreal Protocol can complement other chemical and environmental treaties.

SUBMITTER: Andersen SO

PROVIDER: S-EPMC8665836 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:PurposeMany age-related structural and functional changes in the brain have important consequences. Long-term exposure to mercury and the impact of functional polymorphisms of metal-regulating proteins such as metallothioneins (MTs) can result in neurological-neurobehavioral effects in elderly individuals. Therefore, the aims of this study are to examine the associations between biomarkers of mercury exposure and cognitive impairment and to investigate the effect of the rs8052394 single nucleotide polymorphism (SNP) of the potential modifier gene MT1A on different domains of the Montreal Cognitive Assessment (MoCA).Materials and methodsWe studied 436 participants aged ≥55 years from the Electricity Generating Authority of Thailand study. They underwent a physical examination, an extensive cognitive assessment with the MoCA (cutoff <26 points), and a biochemical analysis related to diabetes and dyslipidemia. The blood mercury level was determined by inductively coupled plasma mass spectrometry. Genotyping of the MT1A rs8052394 SNP was performed by the restriction fragmentation length polymorphism method.ResultsThe mean age of the study population was 58.8±3.01 years, and most had ≥12 years of education (75.7%). The primary study finding was that the prevalence of mild cognitive impairment (MCI) in older Thai adults was 39.7%. The frequency distributions of the G allele of the rs8052394 SNP of the MT1A gene were significantly associated with the total and sub-domain MoCA scores. The prevalence of MCI was significantly associated with increased age, hypertriglyceridemia, hyperhomocysteinemia, the third tertile of blood mercury concentration, and the rs8052394 variant genotype of MT1A (P values for all odds ratios <0.05).ConclusionThese findings suggested that neurocognitive effects associate with mercury exposure and genetic susceptibility in toxicokinetics. Public health strategies can be used to implement as a comprehensive action plan to educate vulnerable populations on how to reduce mercury exposure. Concurrently, impact of such genetic predisposition requires replication for identifying and protecting susceptible individuals from mercury toxicity.

Project description:BackgroundAlthough ozone-depleting methyl bromide was destined for phase-out by 2005, it is still widely applied as a consequence of various critical-use-exemptions and mandatory international regulations aiming to restrict the spread of pests and alien species (e.g. in globalized transport and storage). The withdrawal of methyl bromide because of its environmental risk could fortuitously help in the containment of its human toxicity.MethodsWe performed a systematic review of the literature, including in vitro toxicological and epidemiological studies of occupational and community exposure to the halogenated hydrocarbon pesticide methyl bromide. We focused on toxic (especially chronic) or carcinogenic effects from the use of methyl bromide, on biomonitoring data and reference values. Eligible epidemiological studies were subjected to meta-analysis.ResultsOut of the 542 peer reviewed publications between 1990-2011, we found only 91 referring to toxicity of methyl bromide and 29 using the term "carcinogenic", "neoplastic" or "mutagenic". Several studies provide new additional data pertaining to the mechanistic aspects of methyl bromide toxicity. Few studies have performed a detailed exposure assessment including biomonitoring. Three evaluated epidemiological studies assessed a possible association between cancer and methyl bromide. Overall, exposure to methyl bromide is associated with an increased risk of prostate cancer OR, 1.21; 95% CI (0,98-1.49), P = 0.076. Two epidemiological studies have analyzed environmental, non-occupational exposure to methyl bromide providing evidence for its health risk to the general public. None of the epidemiological studies addressed its use as a fumigant in freight containers, although recent field and case reports do refer to its toxic effects associated with its use in shipping and storage.ConclusionsBoth the epidemiological evidence and toxicological data suggest a possible link between methyl bromide exposure and serious health problems, including prostate cancer risk from occupational and community exposure. The environmental risks of methyl bromide are not in doubt, but also its health risks, especially for genetically predisposed subjects, should not be underestimated.

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Narrowing feedstock exemptions under the Montreal Protocol has multiple environmental benefits.

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