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Chlorinated paraffins (CPs) have become global pollutants and are of considerable concern as a result of their persistence and long-distance transmission in the environment and toxicity to mammals. However, their risks to pollinating insects are unknown. Honeybees are classical pollinators and sensitive indicators of environmental pollution. Herein, the effects of CPs on the gut microenvironment and underlying mechanisms were evaluated and explored using Apis mellifera L. Both short- and medium-chain CPs had significant sublethal effects on honeybees at a residue dose of 10 mg/L detected in bee products but did not significantly alter the composition or diversity of the gut microbiota. However, this concentration did induce significant immune, detoxification, and antioxidation responses and metabolic imbalances in the midgut. The mechanisms of CP toxicity in bees are complicated by the complex composition of these chemicals, but this study indicated that CPs could substantially affect intestinal physiology and metabolic homeostasis. Therefore, CPs in the environment could have long-lasting impacts on bee health. Future studies are encouraged to identify novel bioindicators of CP exposure to detect early contamination and uncover the detailed mechanisms underlying the adverse effects of CPs on living organisms, especially pollinating insects.

Short-chain chlorinated paraffins (SCCPs) have attracted considerable attention for their characteristic of persistent organic pollutants. However, very limited information is available for their toxic effects at environmentally relevant doses, limiting the evaluation of their health risks. In this study, cell viability assay and targeted metabolomic approach was used to evaluate the environmental dose (<100 μg/L) effect of SCCPs on HepG2 cells. Cell viability was found to be decreased with increases in exposure dose of SCCPs. Exposure for 48 h to C10-CPs resulted in a significant reduction in cell viability compared with 24 h, even at 1 μg/L. SCCPs exposure altered the intracellular redox status and caused significant metabolic disruptions. As a kind of peroxisome proliferator, SCCPs specifically stimulated the β-oxidation of unsaturated fatty acids and long-chain fatty acids. Meanwhile, SCCPs exposure disturbed glycolysis and amino acid metabolism, and led to the up-regulation of glutamate metabolism and urea cycle. The toxic effects of SCCPs might mainly involve the perturbation of energy production, protein biosynthesis, fatty acid metabolism, and ammonia recycling.

To study the formation of air pollutants and soot precursors (e.g., acetylene, 1,3-butadiene, benzene, and higher aromatics) from aliphatic and aromatic fractions of gasoline fuels, the Utah Surrogate Mechanisms is extended to include submechanisms of gasoline surrogate compounds using a set of mechanism generation techniques. The mechanism yields very good predictions of species concentrations in premixed flames of n-heptane, isooctane, benzene, cyclohexane, olefins, oxygenates, and gasoline using a 23-component surrogate formulation. The 1,3-butadiene emission comes mainly from minor fuel fractions of olefins and cyclohexane. The benzene formation potential of gasoline components shows the following trends as functions of (i) chemical class: n-paraffins < isoparaffins < olefins < naphthalenes < alkylbenzenes < cycloparaffins < toluene; (ii) carbon number: n-butane < n-pentane < n-hexane; and (iii) branching: n-hexane < isohexane < 2,2,4-trimethylpentane < 2,2,3,3-tetramethylbutane. In contrast, fuel structure is not the main factor in determining acetylene formation. Therefore, matching the benzene formation potential of the surrogate fuel to that produced by the real fuel should have priority when selecting candidate surrogate components for combustion simulations.